Molecular Features of Hormone-Refractory Prostate Cancer Cells by Genome-wide Gene-expression Profiles
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE6811 | GEO | 2007/06/01
SECONDARY ACCESSION(S): PRJNA99185
REPOSITORIES: GEO
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Project description:Seven pairs of hormone sensitive and hormone refractory prostate cancer xenografts
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Project description:In this study we performed transcriptional profiling of transurethral resections of hormone resistant prostate cancer and compared it with benign prostatic hyperplasia (BPH), untreated localized prostate cancer and hormone sensitive prostate cancer. Keywords: time course; disease state analysis
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Project description:Luminal breast cancers express estrogen (ER) and/or progesterone (PR) receptors and respond to hormone therapies. Basal-like “triple negative” (TN) cancers lack steroid receptors but are cytokeratin (CK) 5-positive and require chemotherapy. Here we show that over half of primary ER+PR+ breast cancers contain an ER–PR–CK5+ “luminobasal” subpopulation exceeding 1% of cells. Starting from ER+PR+ luminal cell lines, we generated novel lines with varying luminal to luminobasal-cell ratios and studied their molecular and biological properties. In luminal disease, luminobasal cells expand in response to antiestrogen or estrogen withdrawal therapies. The phenotype and gene signature of the hormone resistant cells matches that of clinical TN basal-like and claudin-low disease. Luminobasal-cell expansion in response to hormone therapies is regulated by Notch1 signaling and can be blocked by gamma-secretase inhibitors (GSI). Our data establish a previously unrecognized plasticity of ER+PR+ luminal breast cancers that, without genetic manipulation, mobilizes outgrowth of hormone-resistant basal-like disease in response to treatment. This undesirable outcome can be prevented by combining endocrine therapies with Notch inhibition. 24 array samples
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