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Links from GEO DataSets

Items: 20

1.

Estrogen receptor coregulator binding modulators (ERXs) effectively target estrogen receptor positive human breast cancers

(Submitter supplied) We examined the transcriptional chagnes modulated by ECBI-11 by perfroming global transcriptome analysis. ZR75 cells were treated with either control or ECBI-11 in the presence of E2 for 48 h and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that ECBI modulated several genes that are involved in cell cycle, breast cancer signaling, estrogen signaling and apoptosis.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
2.

A novel small molecule targeting oncogenic PELP1 demonstrates anti-tumor activity in wild type and mutant estrogen receptor alpha-positive breast cancer

(Submitter supplied) RNA-seq analyses showed SMIP34 treatment altered the expression of genes associated withEstrogen Response, Cell Cycle and Apoptosis pathways
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE199088
ID:
200199088
3.

Genome-wide copy number profiling of MCF-7 and fulvestrant-resistant MCF-7/FR cells by SNP microarray.

(Submitter supplied) Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. more...
Organism:
Homo sapiens
Type:
SNP genotyping by SNP array; Genome variation profiling by SNP array
Platform:
GPL6801
2 Samples
Download data: CEL, CNCHP, TXT
Series
Accession:
GSE121631
ID:
200121631
4.

Fulvestrant withdrawal from fulvestrant-resistant MCF-7/FR cells

(Submitter supplied) Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
24 Samples
Download data: IDAT
Series
Accession:
GSE121379
ID:
200121379
5.

RNA-seq of breast cancer cell lines post ligand treatment II

(Submitter supplied) Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MDA-MB-134 VI, MDA-MB-330, EFM-19, T-47D, and BT-474). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
38 Samples
Download data: TSV
Series
Accession:
GSE128911
ID:
200128911
6.

ATAC-seq, ChIP-seq and RNA-seq of breast cancer cell lines post ligand treatment

(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:
GPL18573 GPL20301
145 Samples
Download data
Series
Accession:
GSE117943
ID:
200117943
7.

RNA-seq of breast cancer cell lines post ligand treatment I

(Submitter supplied) Goal: study the impact of estrogen receptor ligands on gene expression in HR+ breast cancer cells Methods: RNA sequencing Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), promotes transcriptional activation of ER and mimics the transcriptional effect of natural ligand E2 for a subset of ER target genes, consistently across the seven breast cell lines (MCF-7, HCC1500, MDA-MB-330, EFM-19, T-47D, BT-474, and CAMA-1). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
82 Samples
Download data: TSV
Series
Accession:
GSE117942
ID:
200117942
8.

ChIP-seq of ER in MCF-7 cells post ligand treatment

(Submitter supplied) Goal: study the impact of estrogen receptor (ER) ligands on ER binding to chromatin in MCF-7 cells Methods: ER Chromatin Immunoprecipitation and Sequencing (ChIP-seq) Results: All tested ligands increase binding of ER onto DNA in MCF-7 breast cells. These ligands thus promote an association between ER and DNA, irrespective of their mode of action: selective ER modulator (SERM) 4-OH tamoxifen, and selective ER degraders (SERD) fulvestrant and GDC-0927.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: TSV
Series
Accession:
GSE117941
ID:
200117941
9.

ATAC-seq of MCF-7 cells post ligand treatment

(Submitter supplied) Goal: study the impact of estrogen receptor ligands on chromatin accessibility in MCF-7 cells Methods: Assay for Transposase-Accessible Chromatin using Sequencing (ATAC-Seq) Results: Ligand 4-OH tamoxifen, a selective ER modulator (SERM), significantly alters chromatin accessibility and partially mimics the effect of natural ligand E2 on chromatin accessibility in MCF-7 breast cells. Selective ER degraders (SERD) fulvestrant and GDC-0927 on the other hand have very little impact on chromatin accessibility.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: TSV
Series
Accession:
GSE117940
ID:
200117940
10.

AKT antagonist AZD5363 influences estrogen receptor function in endocrine resistant breast cancer and synergizes with fulvestrant (ICI182780) in vivo

(Submitter supplied) Phosphoinositide-3-kinase/protein-kinaseB/mammalian target of rapamycin (PI3K/AKT/mTOR) signalling plays an important role in breast cancer (BC). Its interaction with estrogen receptor (ER) signalling becomes more complex and inter-dependent with acquired endocrine resistance. Targeting mTOR combined with endocrine therapy has shown clinical utility, however, a negative feedback-loop exists downstream of PI3K/AKT/mTOR. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
12 Samples
Download data: TXT
Series
Accession:
GSE69893
ID:
200069893
11.

Effect of RBP2 on MCF7 breast cancer cells (RNA-seq)

(Submitter supplied) RNA-sequencing analysis of RBP2 overexpressing MCF7 cell lines. RBP2 (also known as JARID1A), a member of the JARID1 family of histone H3 lysine K4 demethylases, has been considered to have an oncogenic potential in several cancer including breast cancer. Results provide insight into the transcriptional regulation of RBP2 in estrogen receptor positve breast cancer.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
6 Samples
Download data: TXT
Series
Accession:
GSE92943
ID:
200092943
12.

Genome wide expression change by SMURF1 knocking down in MCF-7 cells

(Submitter supplied) We aim to the investigate the role of SMURF1 in breast cancer progression. MCF-7 cells were used as the model and SMURF1 was silenced by siRNA.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
6 Samples
Download data: FPKM_TRACKING
13.

Cholesterol biosynthesis pathway as a novel mechanism of resistance to estrogen deprivation in estrogen receptor positive breast cancer

(Submitter supplied) Therapies targeting estrogenic stimulation in estrogen receptor positive (ER+) breast cancer (BC) reduce mortality, but resistance remains a major clinical problem. Molecular studies have shown few high frequency mutations to be associated with endocrine resistance. In contrast, expression profiling of primary ER+ BC samples has identified several promising signatures/networks for targeting. In this study, the cholesterol biosynthesis pathway was the common upregulated pathway in the ER+ LTED but not ER- LTED cell lines, suggesting a potential mechanism dependent on continued ER expression. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
54 Samples
Download data: TXT
Series
Accession:
GSE75971
ID:
200075971
14.

ER ChIP-seq of Androstenedione treated Letrozole Resistant Breast Cancer Cell line

(Submitter supplied) Acquired resistance to aromatase inhibitor (AI) therapy is a major clinical problem in the treatment of breast cancer. The detailed mechanisms of how tumour cells develop this resistance remain unclear. Here estrogen receptor ChIPseq analysis identifies adaptations of the ER in response to prolonged letrozole treatment.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL9115 GPL10999 GPL11154
8 Samples
Download data: BED, BEDGRAPH
Series
Accession:
GSE54592
ID:
200054592
15.

Gene expression profiling of breast cancer cells with knockdown of PTEN

(Submitter supplied) Activation of the PI3K pathway in estrogen receptor α (ER)-positive (+) breast cancer is associated with reduced ER expression and activity, luminal B subtype, and poor outcome. PTEN is a negative regulator of the PI3K pathway typically lost in ER-negative (-) breast cancer. To clarify the effect of PTEN down-regulation on the response of ER+/HER2- breast cancer to endocrine therapy, we established reduced PTEN cell models using inducible knockdown. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9052
2 Samples
Download data: FPKM_TRACKING
16.

Synergistic targeting of estrogen-receptor positive breast cancers by MDM2 inhibition in combination with endocrine therapy or CDK4/6 inhibition

(Submitter supplied) Here we characterise the response of models of ER-positive breast cancer to treatment with the small molecule MDM2 inhibitor NVP-CGM097, a dihydroisoquinolinone derivative currently evaluated in a phase I clinical trial. We show that NVP-CGM097 reduces tumour cell viability of in vitro and in vivo models of endocrine sensitive, endocrine resistant and palbociclib (CDK4/6 inhibitor) resistant p53 wildtype (p53wt) ER-positive breast cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
29 Samples
Download data: CSV
17.

Heat Shock Factor 1 (HSF1) regulates ESR1 action in breast cancer

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
12 Samples
Download data: TXT
18.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in 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:
GPL18460
28 Samples
Download data: BED, TXT
Series
Accession:
GSE159803
ID:
200159803
19.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (RNA-seq)

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
18 Samples
Download data: TXT
20.

Heat Shock Factor 1 (HSF1) supports the ESR1 action in breast cancer (ChIP-seq)

(Submitter supplied) Heat shock factor 1 (HSF1) is a key regulator of transcriptional responses to proteotoxic stress. It has been recently linked to signaling of estrogen via ESR1. To study the cooperation of HSF1 and ESR1 in the transcriptional response to estrogen, we established estrogen receptor (ER)-positive breast cancer cell lines with reduced HSF1 levels using specific shRNA or CRISPR/Cas9 approach. HSF1 deficiency led to the inhibition of the mitogenic effect of estrogen in MCF7 and T47D cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18460
10 Samples
Download data: BED, TXT
Series
Accession:
GSE159724
ID:
200159724
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