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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

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
6.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer (xenograft RNA-seq)

(Submitter supplied) Activating estrogen receptor alpha (ER) mutations are present in primary endometrial and metastatic breast cancers, promoting estrogen-independent activation of the receptor. Functional characterizations in breast cancer have established unique molecular and phenotypic consequences of the receptor, yet the impact of ER mutations in endometrial cancer has not been fully explored. In this study, we used CRISPR-Cas9 to model the clinically prevalent ER-Y537S mutation and compared results to ER-D538G to discover allele-specific differences between ER mutations in endometrial cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TXT
Series
Accession:
GSE231744
ID:
200231744
7.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial 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:
GPL24676
32 Samples
Download data: BEDGRAPH, NARROWPEAK
Series
Accession:
GSE205879
ID:
200205879
8.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer (RNA-Seq)

(Submitter supplied) Activating estrogen receptor alpha (ER) mutations are present in primary endometrial and metastatic breast cancers, promoting estrogen-independent activation of the receptor. Functional characterizations in breast cancer have established unique molecular and phenotypic consequences of the receptor, yet the impact of ER mutations in endometrial cancer has not been fully explored. In this study, we used CRISPR-Cas9 to model the clinically prevalent ER-Y537S mutation and compared results to ER-D538G to discover allele-specific differences between ER mutations in endometrial cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE205878
ID:
200205878
9.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer (ChIP-Seq)

(Submitter supplied) Activating estrogen receptor alpha (ER) mutations are present in primary endometrial and metastatic breast cancers, promoting estrogen-independent activation of the receptor. Functional characterizations in breast cancer have established unique molecular and phenotypic consequences of the receptor, yet the impact of ER mutations in endometrial cancer has not been fully explored. In this study, we used CRISPR-Cas9 to model the clinically prevalent ER-Y537S mutation and compared results to ER-D538G to discover allele-specific differences between ER mutations in endometrial cancer. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
13 Samples
Download data: BEDGRAPH, NARROWPEAK
Series
Accession:
GSE205877
ID:
200205877
10.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer (ATAC-Seq)

(Submitter supplied) Activating estrogen receptor alpha (ER) mutations are present in primary endometrial and metastatic breast cancers, promoting estrogen-independent activation of the receptor. Functional characterizations in breast cancer have established unique molecular and phenotypic consequences of the receptor, yet the impact of ER mutations in endometrial cancer has not been fully explored. In this study, we used CRISPR-Cas9 to model the clinically prevalent ER-Y537S mutation and compared results to ER-D538G to discover allele-specific differences between ER mutations in endometrial cancer. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: BEDGRAPH
Series
Accession:
GSE205875
ID:
200205875
11.

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
12.

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
13.

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
14.

Whole-genome DNA methylation profiling of ESR1 Q375H and R394H mutations from the human breast cancer MB-231 stable cells.

(Submitter supplied) Estrogen insensitivity syndrome (EIS) arises from rare mutations in estrogen receptor α (ERα, encoded by ESR1 gene) resulting in the inability of estrogen to exert its biological effects. Due to the rarity, mutations in ESR1 gene and the underlying molecular mechanisms of EIS have not been thoroughly studied. We used human EPIC DNA methylation array to comparison of the transcriptome between the WT ESR1 and Q375H and R394H clinical mutants in MB231 stable cell lines.
Organism:
Homo sapiens
Type:
Methylation profiling by genome tiling array
Platform:
GPL21145
27 Samples
Download data: IDAT
Series
Accession:
GSE139687
ID:
200139687
15.

Whole transcriptome profiling of ESR1 Q375H and R394H mutatons from the human breast cancer MB-231 stable cells

(Submitter supplied) Estrogeh insensitivity syndrome (EIS) arises from rare mutations in estrogen receptor α (ERα, encoded by ESR1 gene) resulting in the inability of estrogen to exert its biological effects. Due to the rarity, mutations in ESR1 gene and the underlying molecular mechanisms of EIS have not been thoroughly studied. We used whole transcriptome analysis to comparison of the transcriptome between the WT ESR1 and Q375H and R394H clinical mutants in MB231 stable cell lines.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL23126
27 Samples
Download data: CEL, CHP
Series
Accession:
GSE139489
ID:
200139489
16.

CRISPR-Cas9 directed modelling of estrogen receptor mutations identified in breast cancer

(Submitter supplied) Estrogen receptor (ER) is the major driver of a large proportion of breast cancers, and many therapies have been designed to target it. These include anti-estrogens, which target ER directly, and aromatase inhibitors, which instead prevent the biosynthesis of estrogen in post-menopausal women. These therapies have been largely successful, but unfortunately many patients eventually succumb to resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
102 Samples
Download data: CSV
17.

Noncoding somatic and inherited single-nucleotide variants converge to promote ESR1 expression in breast cancer

(Submitter supplied) Sustained expression of the estrogen receptor-α (ESR1) drives two-thirds of breast cancer and defines the ESR1-positive subtype. ESR1 engages enhancers upon estrogen stimulation to establish an oncogenic expression program1. Somatic copy number alterations involving the ESR1 gene occur in approximately 1 % of ESR1-positive breast cancers2–5, suggesting that other mechanisms underlie the persistent expression of ESR1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
2 Samples
Download data: TXT
18.

Aberrant claudin-6–adhesion signal promotes endometrial cancer progression via estrogen receptor α

(Submitter supplied) Cell adhesion proteins not only maintain tissue integrity but also possess signaling abilities to organize diverse cellular events in a variety of physiological and pathological processes; however, the underlying mechanism remains obscure. Among cell adhesion molecules, the claudin (CLDN) family often possesses aberrant expression in various cancers, but the biological relevance and molecular basis have not yet been established. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
3 Samples
Download data: TXT
Series
Accession:
GSE161384
ID:
200161384
19.

GATA3 acts upstream of FOXA1 in mediating ER binding by shaping enhancer accessibility

(Submitter supplied) Estrogen Receptor (ESR1) drives growth in the majority of human breast cancers by binding to regulatory elements and inducing transcription events that promote tumor growth. Differences in enhancer occupancy by ESR1, contribute to the diverse expression profiles and clinical outcome observed in breast cancer patients. GATA3 is an ESR1 co-operating transcription factor mutated in breast tumors, however its genomic properties are not fully defined. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
34 Samples
Download data: BED
Series
Accession:
GSE40129
ID:
200040129
20.

GATA3 acts upstream of FOXA1 in mediating ER binding by shaping enhancer accessibility

(Submitter supplied) Estrogen Receptor (ESR1) drives growth in the majority of human breast cancers by binding to regulatory elements and inducing transcription events that promote tumor growth. Differences in enhancer occupancy by ESR1, contribute to the diverse expression profiles and clinical outcome observed in breast cancer patients. GATA3 is an ESR1 co-operating transcription factor mutated in breast tumors, however its genomic properties are not fully defined. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6947
22 Samples
Download data: TXT
Series
Accession:
GSE39623
ID:
200039623
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