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Links from GEO DataSets

Items: 20

1.

RNA-seq analysis of ESR1 mutations in T47D and MCF7 cell lines

(Submitter supplied) Purpose: Transcriptome analysis of ESR1 mutant cells was performed via sequencing total RNA in T47D and MCF7 cell lines containing Y537S and D538G mutations.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
48 Samples
Download data: CSV
2.

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic 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
Platforms:
GPL11154 GPL16791
17 Samples
Download data: WIG
Series
Accession:
GSE78286
ID:
200078286
3.

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [RNA-Seq]

(Submitter supplied) Estrogen receptor-α (ERα) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
11 Samples
Download data: XLSX
4.

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [ChIP-Seq]

(Submitter supplied) Estrogen receptor-α (ERα) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: WIG
Series
Accession:
GSE78284
ID:
200078284
5.

FOXA1 ChIP-seq analysis of genome-edited T47D ESR1 mutant cell models

(Submitter supplied) This study is designed to comprehensively characterize the FOXA1 cistromes of Y537S and D538G mutated ER versus WT ER in breast cancer cells.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: BIGWIG
Series
Accession:
GSE165280
ID:
200165280
6.

ChIP-seq analysis of genome-edited MCF7 and T47D ESR1 mutant cell models

(Submitter supplied) This study is designed to comprehensively characterize the cistromes of Y537S and D538G mutated ER versus WT ER in breast cancer cells. Genome-edited MCF7 and T47D cells were hormone deprived and treated with or without E2 for 45 minuts. Chromatin DNA was then extracted from each sample. The immunoprecipitation was performed using ERα (Santa Cruz Biotechnologies, sc543) antibody. Pooled DNA samples from individual clones were sent to sequencing with Illumina Hiseq 2500 Platform. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BED
Series
Accession:
GSE125117
ID:
200125117
7.

ESR1 mutations affect anti-proliferative responses to tamoxifen through enhanced cross-talk with IGF signaling

(Submitter supplied) The rediscovery of estrogen receptor (ESR1) mutations in metastatic breast cancer is current clinical scenario. We have modeled the three most frequent ESR1 mutations using stable lentiviral vectors in human breast cancer cell lines, and determined that they confer relative resistance to tamoxifen (Tam) in a cell-type specific manner due to distinct epigenetic changes. Resistance was only observed with concomitant engagement and activation of the insulin growth factor signaling pathway (IGF1R). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
23 Samples
Download data: CEL
Series
Accession:
GSE95529
ID:
200095529
8.

Discovery of naturally occurring ESR1 mutations during acquisition of resistance to endocrine therapy in widely used estrogen receptor positive breast cancer cell lines

(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
Platforms:
GPL16791 GPL18573
27 Samples
Download data: XLS
Series
Accession:
GSE100076
ID:
200100076
9.

Discovery of naturally occurring ESR1 mutations during acquisition of resistance to endocrine therapy in widely used estrogen receptor positive breast cancer cell lines [RNA-Seq]

(Submitter supplied) We report the first discovery of naturally occurring ESR1Y537C and ESR1Y537S mutations in MCF7 and SUM44 ESR1-positive cell-lines after acquisition of resistance to long-term-estrogen-deprivation (LTED) and subsequent resistance to fulvestrant (ICIR).
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL16791
15 Samples
Download data: TXT
10.

Discovery of naturally occurring ESR1 mutations during acquisition of resistance to endocrine therapy in widely used estrogen receptor positive breast cancer cell lines [ChIP-Seq]

(Submitter supplied) We report the first discovery of naturally occurring ESR1Y537C and ESR1Y537S mutations in MCF7 and MCF7 ESR1-positive cell-lines after acquisition of resistance to long-term-estrogen-deprivation (LTED) and subsequent resistance to fulvestrant (ICIR).
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: XLS
Series
Accession:
GSE100074
ID:
200100074
11.

Transcriptome Analysis Reveals a Role for Myc in Constitutive and Antiestrogen-resistant Proliferation of Breast Cancer Cells Expressing ERαY537S and ERαD538G Mutations

(Submitter supplied) Approximately 30% of metastatic breast cancers harbor estrogen receptor α (ERα/ESR1) mutations that are associated with resistance to endocrine therapy and shorter patient survival. How these ERα mutations elicit an aggressive tumor phenotype was largely unknown. Recently, we reported cell lines in which the wild-type ESR1 gene is replaced by the two most common ERα mutations, ERαY537S and ERαD538G. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
27 Samples
Download data: TXT
12.

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial 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:
GPL16791
58 Samples
Download data: BEDGRAPH, NARROWPEAK
Series
Accession:
GSE132430
ID:
200132430
13.

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [RNA-seq]

(Submitter supplied) Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: TXT
14.

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ChIP-seq]

(Submitter supplied) Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
22 Samples
Download data: BEDGRAPH, NARROWPEAK
Series
Accession:
GSE132426
ID:
200132426
15.

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ATAC-seq]

(Submitter supplied) Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
20 Samples
Download data: BEDGRAPH
Series
Accession:
GSE132424
ID:
200132424
16.

Evaluating hormone responses in Esr1-wildtype and mutant mammary luminal cells [RNA-seq]

(Submitter supplied) To examine the effects of hormone stimulation on Esr1-wildtype and Esr1-mutant mammary glands, we will ovariectomize both wildtype and ER-mutant mice. Following ovariectomy (OVX), animals will be implanted with hormone pellets (either placebo, estrogen, and/or progesterone). Then, we perform RNA-seq on FACS-sorted mature luminal cells (ML) from mammary glands of treated mice. This analysis will allow for separation of ER mutant-intrinsic effects on gene expression vs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
37 Samples
Download data: TAB
Series
Accession:
GSE186453
ID:
200186453
17.

Evaluating ER-alpha and PR interactions with chromatin in Esr1-wildtype and mutant mammary luminal cells

(Submitter supplied) To understand the interactions between ER-alpha and PR interactions with chromatin in Esr1-wildtype versus mutant mammary cells, ChIP-seq was performed against both transcription factors. Animals were treated for four days with E2 and P4, then harvested for analysis.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
12 Samples
Download data: BIGWIG, NARROWPEAK
Series
Accession:
GSE186452
ID:
200186452
18.

ESR1 fusions invoke breast cancer subtype-dependent enrichment of ligand independent oncogenic signatures and phenotypes

(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
Platforms:
GPL24676 GPL30173
50 Samples
Download data
Series
Accession:
GSE266408
ID:
200266408
19.

ESR1 fusions invoke breast cancer subtype-dependent enrichment of ligand independent oncogenic signatures and phenotypes [ChIP-seq]

(Submitter supplied) Breast cancer is a leading cause of female mortality and despite advancements in personalized therapeutics, metastatic disease largely remains incurable due to drug resistance. The estrogen receptor (ER, ESR1) is expressed in two-thirds of all breast cancer, and under endocrine stress, somatic ESR1 mutations arise in ~30% of cases that result in endocrine resistance. We and others reported ESR1 fusions as a mechanism of ER mediated endocrine resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30173
14 Samples
Download data: CSV
Series
Accession:
GSE266407
ID:
200266407
20.

ESR1 fusions invoke breast cancer subtype-dependent enrichment of ligand independent oncogenic signatures and phenotypes [RNA-seq]

(Submitter supplied) Breast cancer is a leading cause of female mortality and despite advancements in personalized therapeutics, metastatic disease largely remains incurable due to drug resistance. The estrogen receptor (ER, ESR1) is expressed in two-thirds of all breast cancer, and under endocrine stress, somatic ESR1 mutations arise in ~30% of cases that result in endocrine resistance. We and others reported ESR1 fusions as a mechanism of ER mediated endocrine resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
36 Samples
Download data: TXT
Series
Accession:
GSE249723
ID:
200249723
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