Journal
EXPERT REVIEW OF ENDOCRINOLOGY & METABOLISM
Volume 6, Issue 3, Pages 483-493Publisher
ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
DOI: 10.1586/EEM.11.33
Keywords
abiraterone; androgen receptor; cell cycle; hormone therapy; prostatic adenocarcinoma; retinoblastoma
Categories
Funding
- NIH [CA09996, ES16675]
- NATIONAL CANCER INSTITUTE [R01CA099996] Funding Source: NIH RePORTER
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Prostatic adenocarcinomas are reliant on androgen receptor (AR) activity for survival and progression. Therefore, first-line therapeutic intervention for disseminated disease entails the use of AR-directed therapeutics, achieved through androgen deprivation and direct AR antagonists. While initially effective, recurrent, 'castrate-resistant' prostate cancers arise, for which there is no durable means of treatment. An abundance of clinical study and preclinical modeling has led to the revelation that restored AR activity is a major driver of therapeutic failure and castrate-resistant prostate cancer development. The mechanisms underpinning AR reactivation have been identified, providing the foundation for a new era of drug discovery and rapid translation into the clinic. As will be reviewed in this article, these creative new ways of suppressing AR show early promise.
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