Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tamoxifen-associated endometrial tumors expose differential enhancer activity for Estrogen Receptor alpha

ABSTRACT: Tamoxifen-associated endometrial tumors expose differential enhancer activity for Estrogen Receptor alpha

PROVIDER: PRJNA371410 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5198770.fastq.gz	Fastqsanger.gz
	SRR5198780.fastq.gz	Fastqsanger.gz
	SRR5198790.fastq.gz	Fastqsanger.gz
	SRR5198771.fastq.gz	Fastqsanger.gz
	SRR5198781.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Tamoxifen-associated endometrial tumors expose differential enhancer activity for Estrogen Receptor alpha [ChIP-Seq]

Project description:Tamoxifen, a small molecule inhibitor that binds the Estrogen Receptor alpha (ERα), blocks breast cancer progression while increasing the risk for endometrial cancer. In this study, we assessed genome-wide ERα-chromatin interactions in surgical specimens of endometrial tumors from patients who were previously treated for breast cancer with tamoxifen, and endometrial tumors from patients who were treated without tamoxifen. We compared ERα and signal at differential ERα sites in endometrial tumors of nine patients who received tamoxifen with endometrial tumors with six patients who never used tamoxifen. In addition, we performed H3K27ac (a marker for activity) ChIPs on the above mentioned endometrial tumors, and assed this signal at differential ERα sites. Compared to endometrial tumors of non-users, tamoxifen-associated endometrial tumors exposed higher H3K27ac intensities at ERα sites that are enriched in tamoxifen-associated endometrial tumors. Four tamoxifen-associated endometrial tumors that we used in our analysis have been previously published as Tumor A, B, D, and E in GSE81213.

2017-03-06 | GSE94031 | GEO

Tamoxifen-associated endometrial tumors expose differential enhancer activity for Estrogen Receptor alpha [Microarray Expression]

2017-03-07 | GSE94523 | GEO

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

Project description: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. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells.

2019-06-11 | GSE132428 | GEO

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

2019-06-11 | GSE132426 | GEO

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

2019-06-11 | GSE132424 | GEO

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer

Project description:Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer

| PRJNA548072 | ENA

Endometrial profile of low-dose estradiol and tamoxifen combination therapy

Project description:Combination therapy with estrogen and a selective estrogen receptor modulator (SERM) is a promising approach to safely alleviate important side effects related to estrogen deficiency in women at high risk for breast cancer. Data related to endometrial safety of estrogen+SERM co-therapies are limited, however. The primary goal of this study was to evaluate the endometrial profile of low-dose E2 and Tam alone and in combination. In this study 16 postmenopausal female cynomolgus macaques were randomized to receive placebo, low-dose micronized estradiol (E2, 0.25 mg/1800 kcal), the SERM tamoxifen (Tam, 20 mg/1800 kcal), or E2+Tam in a parallel-arm design. Endometrial samples were collected after 4 months of treatment and used for microarray analysis.

2010-05-06 | E-GEOD-14518 | biostudies-arrayexpress

Endometrial cancer FFPE tissue SWATH-MS study

Project description:A specific form of endometrial cancer (EC) can develop in breast cancer patients previously treated with tamoxifen (ET), an antagonist of estrogen receptor (ER) α that inhibits proliferation of ER positive breast cancer. ET tumors have a different phenotype than endometrial tumors which typically develop de novo without previous exposure to tamoxifen (EN). Here we aimed to identify specific protein markers that could serve as specific molecular targets in either phenotype. A set of total 45 formalin-fixed paraffin-embedded (FFPE) endometrial tumor tissue and adjacent myometrial tissue samples were analyzed using LC-MS/MS in SWATH-MS mode. We found that calcyphosin (CAPS) levels were elevated in EN tumors compared to ET tumors. The higher CAPS level in EC tissue invading to myometrium support its relationship to EC aggressiveness. Further, stathmin (STMN1) levels were found significantly elevated in ET vs. EN tumors and significantly associated with patient survival. This finding connects elevated levels of this cell cycle regulating, proliferation-associated protein with tamoxifen exposure. In a summary, using SWATH-MS we show that CAPS and STMN1 should be recognized as clinicopathologically different EC markers of which STMN1 is specifically connected with a previous tamoxifen exposition.

2020-05-05 | PXD017217 | Pride

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

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

| PRJNA548067 | ENA

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

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

| PRJNA548065 | ENA