Response of prostate cancer to addition of dutasteride after progression on abiraterone  

作　　者：Jian-Po Lian Yuan-Yuan Gao Jing-Jie Tang Xi Chen Ying Liu Deng-Long Wu Zhen-Fei Li Sheng-Song Huang 

机构地区：[1]Department of Urology,Tongji Hospital,Tongji University School of Medicine,Shanghai 200065,China [2]State Key Laboratory of Cell Biology,Shanghai Institute of Biochemistry and Cell Biology,Center for Excellence in Molecular Cell Science,Chinese Academy of Sciences,University of Chinese Academy of Sciences,Shanghai 200031,China

出　　处：《Asian Journal of Andrology》2021年第2期222-223,共2页亚洲男性学杂志（英文版）

基　　金：This research was partially funded by the National Key R&D program of China(2018YFA0508200 to ZFL);Clinical Innovations of Shanghai SHENKANG(SHDC12019112 to DLW);the Strategic Priority Research Program of Chinese Academy of Sciences(XDB19000000 and XDA12010318 to ZFL);the National Natural Science Foundation of China(81672526 to DLW and 81872075 to JJT);the Prostate Cancer Foundation Young Investigator Award(#15YOUN11 to ZFL).

摘　　要：Dear Editor,Abiraterone has achieved great success in clinic by targeting cytochrome P45017A1(CYP17A)for prostate cancer therapy.1,2 However,drug resistance is inevitable and novel strategy is urgently required.Our previous work unveils a steroidal metabolic pathway for abiraterone in patients.3,4 Steroidogenic enzyme 3β-hydroxysteroid dehydrogenase 1(3βHSD1)catalyzes abiraterone toΔ4-abiraterone(D4A),which is further catalyzed to 5α-abiraterone(5α-Abi)by steroid-5α-reductase(SRD5A).The metabolite 5α-Abi binds to androgen receptor(AR)directly and activates AR signaling.

关 键 词：ABIRATERONE CYP17 cancer 

分 类 号：R697[医药卫生—泌尿科学]