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H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

ABSTRACT: H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

PROVIDER: PRJNA417235 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6260490.fastq.gz	Fastqsanger.gz
	SRR6260500.fastq.gz	Fastqsanger.gz
	SRR6260491.fastq.gz	Fastqsanger.gz
	SRR6260501.fastq.gz	Fastqsanger.gz
	SRR6260492.fastq.gz	Fastqsanger.gz

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Similar Datasets

H3K27Ac in MCF7 Y537S ER mutant cells and RNAseq with and without treatment with THZ1

Project description:H3K27Ac ChIP-seq in MCF7 Y537S ER mutant cells RNAseq analysis of MCF7 Y537S ER mutant cells treated with veh and THZ1

2018-02-15 | GSE106552 | GEO

Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells

Project description:Analysis of MCF7 cells transfected with ER mutants (S463P, Y537S and D538G) in phenol-red free, charcoal stripped FBS media and regular DMEM/F12 media. Results provide insight on the gene expression profiles induced by the various ER mutants. Total RNA extracted from transfected cells 48 hours after transfection 36 samples were analyzed, triplicates for each constructs (GFP vector control, WT, S463P, Y537S, D538G and S463P/D538G) for each type of media

2013-10-25 | E-GEOD-51448 | biostudies-arrayexpress

Gene expression analysis of estrogen receptor mutants, S463P, Y537S and D538G in MCF7 cells

2013-10-25 | GSE51448 | GEO

Effect of diptoindonesin G on T47D cells overexpressing the Y537S ER mutation

Project description:To investigate the effect of diptoindonesin G on breast cancer cells expressing the estrogen receptor Y537S ligand binding domain mutation, we treated T47D cells overexpressing the ER Y537S mutation and treated them with vehicle or diptoindonesin G and performed differential gene expression analysis and gene set enrichment analysis

2022-06-11 | GSE205716 | GEO

ESR1 Y537S and D538G mutations drive resistance to CDK4/6 inhibitors in estrogen receptor-positive breast cancer

Project description:Purpose: Breast cancers with ESR1 mutations are resistant to antiestrogen therapy. We aimed to investigate the association of ESR1 mutations with resistance to CDK4/6 inhibitors (CDK4/6i) using real-world data analysis and experimental validation. Patients and Methods: A total of 3,958 patients with estrogen receptor-positive (ER+) metastatic breast cancer with DNA sequencing data were analyzed. Breast tumor DNA and circulating tumor (ct) DNA were sequenced using the Tempus xT tumor assay and Tempus xF liquid biopsy, respectively. Patients were stratified into either treated with CDK4/6i (breast tumors: 1,070; ctDNA: 1,885) or CDK4/6i naïve (breast tumors: 750; ctDNA: 253). Engineered MCF7 cells carrying ESR1 Y537S or D538G knock-in mutations were used to study antitumor efficacy of the CDK4/6i, palbociclib in vitro and in vivo. Results: In both xF and xT assays, ESR1 mutations were the only somatic alterations significantly more frequent in those who received CDK4/6i than those who did not. Knock-in of ESR1 Y537S or ESR1 D538G in MCF7 cells resulted in upregulation of cell cycle-related gene signatures upon treatment with CDK4/6i ± antiestrogen compared to cells with non-mutant ESR1. MCF7 xenografts harboring ESR1 Y537S and D538G mutations established in nude mice were resistant to palbociclib. Conclusions: We report herein real-world and preclinical evidence that ESR1 mutations, particularly Y537S and D538G, can drive resistance to CDK4/6 inhibitors.

2024-11-12 | GSE281302 | GEO

Knockdown of GRHL2 affects active enhancers (H3K27ac sites) enriched for ER binding

Project description:Differential ChIP-Seq data monitoring changes in active enhancer marks (H3K27ac sites) after treatment with siGRHL2 in MCF7 and T47D breast cancer models. Comparing sites altered by treatment with siGRHL2 after 48hours revealed these sites to be enriched for Estrogen Receptor (ER) binding.

2018-12-07 | GSE123475 | GEO

ER-RIME in wt-MCF7 and MCF7-LTED

Project description:Wild type (wt) MCF7 cells, modelling breast cancer at primary diagnosis, were cultured in phenol red-free RPMI supplemented with 10% FBS and 1nM estradiol (E2). Long-term oestrogen deprived (LTED) cell lines, which model resistance to endocrine therapy, were cultured in phenol red-free RPMI in the absence of exogenous E2 and supplemented with 10% dextran charcoal-stripped bovine serum (DCC). Samples were harvested at baseline and at the point of resistance (LTED). In order to do comparative analysis in the ER-interactome of wt-MCF7 and MCF7-LTED cells, ER-RIME (rapid immunoprecipitation mass spectrometry of endogenous proteins) was conducted in these cells.

2020-07-13 | PXD004648 | Pride

ER ChiP-Seq Mcf7 10nM E2

Project description:ER ChiP-Seq Mcf7 10nM E2

| PRJNA480204 | ENA

Genome-wide analysis of transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

Project description:We analyzed the chromatin state of MDA-MB-453 cells expressing wild-type, Y537S, or K303R ER alpha by ATAC-seq, and identified K303R-related disordered chromatin opening which has Fox-binding motifs.

2022-12-16 | GSE191057 | GEO

Genome-wide analysis of ectopically expressed wild-type, Y537S, or K303R ER alpha-binding genomic regions in MDA-MB-453 cells.

Project description:We analyzed the wild-type, Y537S, or K303R ER alpha-binding genomic regions ectopically expressed in MDA-MB-453 cells by ChIP-seq, and identified K303R-related disordered ERa binding and chromatin opening at Fox motif regions.

2022-12-16 | GSE191058 | GEO

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