Mechanisms of drug resistance that target the androgen axis in castration resistant prostate cancer (CRPC)
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- 作者：Trevor M. Penning ; penning@upenn.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：ADMET ; absorption distribution ; metabolism ; elimination and toxicity ; 螖4-A ; 4-androstene-3 ; 17-dione ; 螖5-Adiol ; 5-androstene-3尾 ; 17尾-diol ; 3伪-Adiol ; 5伪-androstane-3伪 ; 17尾-diol ; Adione ; 5伪-androstane-3 ; 17-dione ; ADT ; androgen deprivation therapy ; AR ; androgen receptor ; AR-FL ; androgen receptor full length ; AR-SV ; androgen receptor splice variant ; CRPC ; castration resistant prostate cancer ; DHEA ; dehydroepiandrosterone ; DHT ; 5伪-dihydrotestosterone ; 3伪-diol ; 5伪-androstane-3伪 ; 17尾-diol ; HSD ; hydroxyster
- 刊名：Journal of Steroid Biochemistry and Molecular Biology
- 出版年：2015
- 出版时间：September 2015
- 年：2015
- 卷：153
- 期：Complete
- 页码：105-113
- 全文大小：758 K
文摘
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Abiraterone and enzalutamide in castration resistant prostate cancer lead to drug resistance.
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Intrinsic drug resistance arises due to allelic variants in organic anion transporters and HSD3B1.
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Acquired drug resistance arises due to intratumoral androgen biosynthesis and changes in the AR.
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Acquired resistance can involve the induction of AKR1C3 and emergence of AR-splice variants.
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AKR1C3 inhibitors or peptidomimetics that block AR-splice variants may surmount drug resistance.