GEO DataSets

Analysis of fulvestrant-sensitive MCF7-R73 cells retrovirally induced with various zinc finger transcription factors. Six unique ZF-TFs conferred stable fulvestrant-resistance. Results provide insight into molecular mechanisms underlying acquired fulvestrant-resistance in breast cancer cells.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 7 genotype/variation, 2 infection sets

Platform:

GPL570

Series:

GSE27444

14 Samples

Download data: CEL

(Submitter supplied) Multiple gene expression studies have demonstrated that breast cancer biological diversity is associated with distinct transcriptional programs. Transcription factors, because of their unique ability to coordinate the expression of multiple genes, are speculated to play a role in generating phenotypic plasticity associated with cancer progression including acquired drug resistance. Combinatorial libraries of artificial zinc-finger transcription factors (ZF-TFs) provide a robust means for inducing and understanding various functional components of the cancer phenotype. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4074

Platform:

GPL570

14 Samples

Download data: CEL

(Submitter supplied) Full title: Expression data from antisense miRNA-221/222 (si221/222) and control inhibitor (GFP) treated fulvestrant-resistant breast cancer cells The expression of miR-221/222 were found to be upregulated in fulvestrant resistant breast cancer cells MCF7-FR compared to its drug-sensitive counterpart MCF7. To investigate the role of miR-221/222 in acquired resistance to fulvestrant, we lowered the level of miR-221/222 in MCF7-FR cells using miRNA inhibitors (antagomirs), and compared gene expression profiles before and after treatment.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4054

Platform:

GPL570

9 Samples

Download data: CEL

Analysis of fulvestrant-resistant MCF7 cells transfected with antisense miRNA inhibitors targeting miR-221 and miR-222. miR-221/222 knockdown inhibits cell proliferation in fulvestrant-resistant MCF7-F cells. Results provide insight into the role of miR-221/222 in acquired resistance to fulvestrant.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 3 genotype/variation sets

Platform:

GPL570

Series:

GSE19777

9 Samples

Download data: CEL

(Submitter supplied) Emergence of antiestrogen-resistant cells in MCF-7 cells during suppression of estrogen signaling is a widely accepted model of acquired breast cancer resistance to endocrine therapy. To obtain insight into the genomic basis of endocrine therapy resistance, we characterized MCF-7 monoclonal sublines that survived 21-day exposure to tamoxifen (T-series sublines) or fulvestrant (F-series sublines) and sublines unselected by drugs (U-series). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

30 Samples

Download data: CEL

(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

(Submitter supplied) Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Keywords: 17b-estradiol responsive genes, OHT resistance, Fulvestrand resistance

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

24 Samples

Download data

(Submitter supplied) Purpose: Resistance to endocrine therapy in estrogen receptor-positive (ER+) breast cancer remains a major clinical problem. Recently, the CDK4/6 inhibitor palbociclib combined with letrozole was approved for treatment of ER+ advanced breast cancer, and other CDK4/6 inhibitors are being investigated in combination with different endocrine treatments. However, the role of CDK4/6 in endocrine resistance and their potential as predictive biomarkers of endocrine treatment response remains undefined. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

26 Samples

Download data: CEL

(Submitter supplied) Trial 223 was a placebo-controlled trial of neoadjuvant anastrozole alone or with gefitinib in early breast cancer. We used patients from arm B and C: anastrozole 1mg/d for the duration of the 16 week period plus placebo 1 tablet/d orally for 2 weeks. Patients in arm B were followed by gefitinib 250mg/d orally for 14 weeks whereas patients in arm C continued with placebo for 14 weeks.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

96 Samples

Download data: CEL

(Submitter supplied) The NEWEST (Neoadjuvant Endocrine Therapy for Women with Estrogen-Sensitive Tumours) trial compared the clinical and biological activity of fulvestrant 500 mg vs 250 mg in the neoadjuvant setting. In this multi-centre phase II study, post-menopausal women with operable, locally advanced (T2, 3, 4b; N0-3; M0) ER-positive breast tumours were randomised to receive neoadjuvant treatment with either dose of fulvestrant for 16 weeks before surgery. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

42 Samples

Download data: CEL

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

65 Samples

Download data: CEL

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

14 Samples

Download data: CEL, XLS

(Submitter supplied) To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

51 Samples

Download data: CEL, TXT

(Submitter supplied) Background: Invasive lobular breast carcinoma (ILC) is a histological subtype of breast cancer that is characterized by loss of E-cadherin, and high expression of estrogen receptor alpha (ER). Many patients with ILC are effectively treated with adjuvant aromatase inhibitors (AIs), however, acquired AI resistance remains a significant problem. Methods: To identify underlying mechanisms of acquired antiestrogen resistance in ILC, we developed a total of 6 long-term estrogen-deprived (LTED) variant cell lines of the human ILC cell lines SUM44PE (SUM44; 2 lines) and MDA-MB-134VI (MM134; 4 lines). more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

27 Samples

Download data: CSV

(Submitter supplied) Although estrogen receptor (ER) and insulin-like growth factor (IGF) signaling are important for normal mammary development and breast cancer, cross-talk between these pathways, particularly at the level of gene transcription, remains poorly understood. We performed microarray analysis on MCF-7 breast cancer cells treated with estradiol (E2) or IGF-I for 3hr or 24hr. IGF-I regulated mRNA of 5-10-fold more genes than estradiol, and many genes were co-regulated by both ligands. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4063

Platform:

GPL571

17 Samples

Download data: CEL

Analysis of MCF-7 breast cancer cells treated with estradiol (E2) or insulin-like growth factor I (IGF-I) for up to 24 hours. E2 and IGF-I signaling are important for normal mammary development and breast cancer. Results provide insight into the cross-talk between these pathways.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 3 agent, 2 time sets

Platform:

GPL571

Series:

GSE26834

17 Samples

Download data: CEL

(Submitter supplied) A significant fraction of breast cancers exhibit de novo or acquired resistance to estrogen deprivation. A kinome-wide siRNA screen identified a role for Insulin Receptor (InsR) in the hormone-independent growth of ER+ breast cancer cells We used gene expression microarrays to identify genes and pathways that are altered by insulin stimulation of ER+ MCF-7 human breast cancer cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13158

9 Samples

Download data: CEL, CHP

(Submitter supplied) Hormone therapy targeting estrogen receptor (ER) is the principal treatment for ER-positive breast cancers but many cancers develop resistance to anti-estrogens. Cyclin-dependent kinase 8 (CDK8) is a transcriptional regulator of several oncogenic pathways. Expression levels of CDK8 and ERα are inversely correlated in breast cancers suggesting a functional association between CDK8 and ER. CDK8 inhibition by selective small-molecule inhibitors, by shRNA knockdown or by CRISPR-Cas9 knockout suppressed estrogen-induced transcription, with no significant effects on ERα protein expression or phosphorylation. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL14550

4 Samples

Download data: TXT, XLSX