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Links from GEO DataSets

Items: 20

1.

MSK1 regulates luminal cell differentiation and metastatic dormancy in breast cancer

(Submitter supplied) For many breast cancer (BCa) patients, symptomatic bone metastases appear after years or even decades of la­tency. How metastatic cells disseminate, and how micromet­astatic lesions remain dormant and undetectable yet initiate colonization, are major questions in cancer research. Here we identify and func­tionally analyse a molecular mechanism involved in bone metastatic latency of estrogen receptor–positive (ER)+ BCa. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: BEDGRAPH
Series
Accession:
GSE100306
ID:
200100306
2.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (RNA-seq II)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
32 Samples
Download data: TXT
3.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ChIP-seq II)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
17 Samples
Download data: BW
Series
Accession:
GSE140185
ID:
200140185
4.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL11154
103 Samples
Download data: BW
Series
Accession:
GSE124228
ID:
200124228
5.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (RNA-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: TXT
6.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ChIP-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: BW
Series
Accession:
GSE124225
ID:
200124225
7.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ATAC-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
20 Samples
Download data: BW
Series
Accession:
GSE124224
ID:
200124224
8.

Non-linear relationship between chromatin accessibility and estradiol-regulated gene expression

(Submitter supplied) Chromatin accessibility is central to basal and inducible gene expression. Through ATAC-seq experiments in Estrogen Receptor-positive (ER+) breast cancer cell line MCF-7 and integrationvwith multi-omics data, we found that estradiol (E2) induced chromatin accessibility changes in the widely studied E2-regulated genes. As expected, open chromatin regions associated with E2-inducible gene expression showed enrichment of estrogen response element and those associated with E2-repressible gene expression were enriched for PBX1, PBX3, and ERE. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL20301
15 Samples
Download data: BW, TXT
Series
Accession:
GSE144580
ID:
200144580
9.

GATA3 mutation disrupts functional network governed by Estrogen receptor, FOXA1 and GATA3

(Submitter supplied) Estrogen Receptor (ER) is a steroid hormone receptor that regulates epithelial genes in breast cancer. ER forms a regulatory network with the other transcription factors, FOXA1 and GATA3. GATA3 is known to be capable of specifying chromatin localization of FOXA1 and ER. GATA3 has been identified as one of the most frequently mutated genes in breast cancer. However, how GATA3 mutations impact this transcriptional network is unknown. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: BIGWIG
Series
Accession:
GSE130703
ID:
200130703
10.

A class of GATA3 mutation reprograms the breast cancer transcriptional network through gain and loss of function

(Submitter supplied) A pioneer transcription factor, GATA3, is one of the most frequently mutated genes in breast cancer, yet the impact of these mutations is largely unknown. We generated a GATA3 mutant cell line (T47D wt/R330fs) by CRISPR. Mutation of one allele of GATA3 led to loss of binding and decreased expression at a subset of genes, including Progesterone Receptor. At other loci, associated with epithelial to mesenchymal transition, gain of binding at a novel sequence motif correlated with increased gene expression. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
96 Samples
Download data: TXT
11.

A shared transcriptional program in early breast neoplasias despite genetic and clinical distinctions

(Submitter supplied) The earliest recognizable stages of breast neoplasia are lesions that represent a heterogeneous collection of epithelial proliferations currently classified based on morphology. Their role in the development of breast cancer is not well understood but insight into the critical events at this early stage will improve efforts in breast cancer detection and prevention. These microscopic lesions are technically difficult to study so very little is known about their molecular alterations. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing
Platform:
GPL10999
72 Samples
Download data: TXT
12.

PDEF knockdown and overexpression in mammary epithelial cells

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
10 Samples
Download data: CEL
Series
Accession:
GSE40987
ID:
200040987
13.

Gene expression profiles induced by overexpression of PDEF in MCF10A mammary epithelial cell line

(Submitter supplied) Recent studies suggest that PDEF is required for secretory cell differentiation in several epithelial tissues. To investigate PDEF in the mammary gland, we examined the effect of this transcription factor on gene expression using microarray based profiling of MCF-10A cells. These cells are non-transformed mammary epithelial cells that express protein and gene expression programs of basal epithelial cells and undetectable levels of endogenous PDEF. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE40986
ID:
200040986
14.

Gene expression profiles induced by shRNA-mediated knockdown of PDEF in MCF7 mammary epithelial cell line

(Submitter supplied) Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
4 Samples
Download data: CEL
Series
Accession:
GSE40985
ID:
200040985
15.

FOXA1 overexpression mediates endocrine resistance by increasing IL-8 in oestrogen receptor-positive breast cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9052
17 Samples
Download data: BED, TXT
Series
Accession:
GSE75372
ID:
200075372
16.

Gene expression profiling of tamoxifen-resistant breast cancer MCF7L cells

(Submitter supplied) Endocrine resistance is a major obstacle in treating estrogen receptor α (ER)-positive (+) breast cancer. In order to better understand the mechanism of endocrine resistance, we established a stable tamoxifen-resistant (TamR) MCF7L cell model by culturing the parental (P) MCF7L cells in the presence of 100 nM of 4-hydroxytamoxifen (4HT) for over 6 months. To characterize the transcriptomic profiles in these cells, we performed an RNA-seq analysis.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9052
2 Samples
Download data: TXT
17.

Gene expression profiling of parental and TAMR MCF7 cells after knock-down of ER or FOXA1 or overexpresion of FOXA1

(Submitter supplied) Gene expression profiles (RNA seq of parental MCF7 cells and tamoxifen resistant cells after ER or FOXA1 knock down and after overexpression of FOXA1 in parenatl cells).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9052
11 Samples
Download data: TXT
18.

CHIP-SEQ of FOXA1 in parental MCF7 cells and tamoxifen resistant MCF7 cells

(Submitter supplied) ChIP sequencing of FOXA1 in MCF7 cells and tamoxifen resistant MCF7 cells
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9052
4 Samples
Download data: BED
Series
Accession:
GSE75201
ID:
200075201
19.

Breast cancer metastasis to gynecological organs – a clinico-pathological and molecular profiling study.

(Submitter supplied) Breast cancer metastasis to gynecological organs is an understudied pattern of tumor spread. We explored clinico-pathologic and molecular features of these metastases to better understand this unique pattern of dissemination.
Organism:
Homo sapiens
Type:
Genome variation profiling by genome tiling array
Platform:
GPL10150
26 Samples
Download data: TXT
Series
Accession:
GSE115080
ID:
200115080
20.

Bone metastatic variant of MCF7 cells

(Submitter supplied) A bone-metastatic variant of MCF7 cells was created from a spontaneous metastasis from the mammary fat pad to the bone marrow in the absence of exogenous estrogen. The goal of the study was to determine differences in gene expression between the parental MCF7 cells and the bone metastatic variant.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
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