Prostate cancer-from steroid transformations to clinical translation

Kai Hsiung Chang, Nima Sharifi

Research output: Contribution to journalReview articlepeer-review

11 Scopus citations

Abstract

The survival benefit conferred by two hormonal agents in phase III trials has clinically validated the long suspected and now widely recognized phenomenon of castration-resistant prostate cancer (CRPC) hormone dependence. Abiraterone inhibits steroid 17-hydroxylase/17,20-lyase (CYP17A1) and blocks androgen synthesis, whereas enzalutamide directly binds and antagonizes the androgen receptor. Both agents are highly effective against CRPC and significantly prolong survival following docetaxel treatment. However, this clinical validation of the androgen pathway has led to questions regarding the fundamental mechanisms of CRPC, as well as resistance to abiraterone and enzalutamide. Our understanding of the predominant steroid transformation pathways that lead to dihydrotestosterone synthesis in CRPC is evolving. The role of steroidogenesis in the development of resistance to abiraterone and enzalutamide remains uncertain. The specific roles of candidate enzyme targets in the development of resistance to these agents must be defined if we are to identify novel targets for improved pharmacologic therapies.

Original languageEnglish (US)
Pages (from-to)721-724
Number of pages4
JournalNature Reviews Urology
Volume9
Issue number12
DOIs
StatePublished - Oct 2 2012

ASJC Scopus subject areas

  • Urology

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