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Expression profiling of response to first-line aromatase inhibitor therapy

ABSTRACT: Fresh-frozen primary cancer specimens of 107 breast cancer patients whose metastases were treated with first-line aromatase inhibitors were evaluated for their whole genome mRNA expression profiles.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41994 | GEO | 2013/12/05

SECONDARY ACCESSION(S): PRJNA178932

REPOSITORIES: GEO

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Expression profiling of response to first-line aromatase inhibitor therapy

Project description:Fresh-frozen primary cancer specimens of 107 breast cancer patients whose metastases were treated with first-line aromatase inhibitors were evaluated for their whole genome mRNA expression profiles. Primary breast tumors (107) were analyzed against a common breast cancer reference pool (BRP).

2013-12-05 | E-GEOD-41994 | biostudies-arrayexpress

microRNA expression profiling of response to first-line aromatase inhibitor therapy

Project description:The main goal of the study is to define miR expression levels related to clinical and biological parameters. Now in particular, miR expression levels of fresh frozen (estrogen receptor-positive) primary tumors were related to PIK3CA genotype and with progression-free survival in breast cancer patients with metastatic breast cancer that received first-line aromatase inhibitor therapy.

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Expression data from 5 colorectal cancer patients neoadjuvantly treated with Imatinib (ImPACCT study)

Project description:Gene expression profiling of CMS4 colon cancer treated with Imatinib in the ImPACCT study. Fresh-frozen biopsies were taken during diagnostic colonoscopy for CMS4 identification. Five patients gave informed consent for two week of neoadjuvant Imatinib therapy prior to removal of the primary tumor. Fresh-frozen samples were taken from surgically resected colon cancer specimens.

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Project description:To identify the genes which have relation to aromatase-inhibitor-resistance, we compared the gene expression of aromatase-inhibitor-resistant cell, A3, with that of parent cell line, T-47D.

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GDNF-RET signaling as a target in aromatase inhibitor resistant breast cancers

Project description:Understanding the complex molecular mechanisms underlying resistance to endocrine therapy is a major challenge in the treatment of estrogen receptor-positive (ER+) breast cancers. We have previously demonstrated that glial cell line-derived neurotrophic factor (GDNF) signaling via the receptor tyrosine kinase RET promotes estrogen independent activation of ER. Here we have addressed the relevance of GDNF-RET signaling in response to aromatase inhibitor treatment and explored the efficacy of using RET inhibitors in breast cancer models of aromatase inhibitor response and resistance. A GDNF-response gene set, identified from gene expression profiling, was demonstrated to be an independent prognostic marker of poor patient outcome and, importantly, to be predictive of poor response to aromatase inhibitor treatment and development of resistance. The relevance of these findings was validated first by demonstrating an association of RET protein expression in an independent cohort of aromatase inhibitor resistant patient samples. Second, in in vitro models, GDNF-mediated RET signaling was demonstrated to enhance the survival of aromatase inhibitor resistant cells and to increase resistance in aromatase inhibitor sensitive cells. These effects could be reversed by targeting GDNF/RET signaling with the RET selective inhibitor NVP-BBT594 thus identifying GDNF-RET signaling as a potential therapeutic target, particularly in breast cancers resistant to aromatase inhibitors.<br>MCF7 cells were E2-deprived by culturing in phenol red-free RPMI 1640 supplemented with 10% DCC for 3 days and then serum-starved overnight in the presence or absence of fulvestrant (ICI182,780) (100 nM). The following day, cells were treated with GDNF (20 ng/ml) for 0, 4, 8, 24 and 48 hours in the presence or absence of fulvestrant (ICI182,780) (100 nM).

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Transcription profiling of human estrogen receptor positive MCF7 cells stably transfected with aromatase gene treated with testosterone, 17 B-estradiol, two aromatase inhibitors (letrozole and anastrozole), and an anti-estrogen (tamoxifen)

Project description:Anti-estrogens and aromatase inhibitors are important drugs in the treatment of estrogen-dependent breast cancer. In order to investigate the effects of these drugs on gene expression in breast cancer cells, we treated estrogen receptor-positive MCF-7 cells, stably transfected with the aromatase gene (known as MCF-7aro cells), with testosterone, 17Î²-estradiol, two aromatase inhibitors (letrozole and anastrozole), and an anti-estrogen (tamoxifen). Microarray analyses using Affymetrix Human Genome U133A GeneChips were carried out using total RNA isolated from the control and treated cells. When comparing the effect of each inhibitor on gene expression we observe that letrozole and anastrozole are more similar in terms of the genes they affect, compared to treatment with tamoxifen. The results of this study provide us with a better understanding of the actions of both aromatase inhibitors and anti-estrogens at the molecular level. We believe that the results of this study serve as the first step in identifying unique expression patterns following drug treatment, and that this will ultimately be useful in customizing patient treatment strategies for estrogen-dependent breast cancer. The data presented here have been processed using the R-Project Bioconductor statistical tools package using the affy library. The following were applied: RMA background correction, pmonly probe-level correction, quantile normalization, avgdiff summary method. Raw data is provided in the form of .CEL files.

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Transcription profiling of human breast cancer biopsies taken before and after patients were treated with aromatase inhibitors

Project description:Molecular response to Aromatase Inhibitor Treatment in Primary Breast Cancer

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Lacrimal Gland Gene expression in Aromatase Knockout Mice and Wild Type Controls

Project description:The Effect of Aromatase Knockout on Gene Expression in the Mouse Lacrimal and Meibomoan Gland. Keywords: Aromatase Knockout vs Wild Type Control

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