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Article

Targeting AR Variant-Coactivator Interactions to Exploit Prostate Cancer Vulnerabilities.

Molecular cancer research : MCR - 1 Nov 2017

Magani Fiorella, Peacock Stephanie O, Rice Meghan A, Martinez Maria J, Greene Ann M, Magani Pablo S, Lyles Rolando, Weitz Jonathan R, Burnstein Kerry L

Abstract excerpt

Castration-resistant prostate cancer (CRPC) progresses rapidly and is incurable. Constitutively active androgen receptor splice variants (AR-Vs) represent a well-established mechanism of therapeutic resistance and disease progression. These variants lack the AR ligand-binding domain and, as such, are not inhibited by androgen deprivation therapy (ADT), which is the standard systemic approach for advanced prostate...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Gene Expression Regulation, Neoplastic

Share to Prostatic Neoplasms, Castration-Resistant

Share to Proto-Oncogene Proteins c-vav

Share to Receptors, Androgen

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Source

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Identifiers

PMID: 28811363
DOI: 10.1158/1541-7786.MCR-17-0280
PMCID: PMC5770277

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