Targeting the Androgen Receptor

被引：50
作者：
Friedlander, Terence W. [1 ]
Ryan, Charles J. [1 ]
机构：
[1] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, Div Genitourinary Med Oncol, San Francisco, CA 94143 USA
来源：
UROLOGIC CLINICS OF NORTH AMERICA | 2012年 / 39卷 / 04期
关键词：
Castration-resistant prostate cancer; Androgen receptor; Abiraterone acetate; Orteronel; Galeterone; MDV3100; ARN-509; EPI-001; INDEPENDENT PROSTATE-CANCER; TUMOR-CELL LINES; ANTIANDROGEN WITHDRAWAL; PHASE-III; DEPRIVATION THERAPY; HORMONAL-THERAPY; GROWTH-FACTOR; OPEN-LABEL; CASTRATION; ACTIVATION;
D O I：
10.1016/j.ucl.2012.07.003
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
Androgen receptor (AR)-mediated signaling is critical to the growth and survival of prostate cancer. Although medical castration and antiandrogen therapy can decrease AR activity and lower PSA, castration resistance eventually develops. Recent work exploring the molecular structure and evolution of AR in response to hormonal therapies has revealed novel mechanisms of progression of castration-resistant prostate cancer and yielded new targets for drug development. This review focuses on understanding the mechanisms of persistent AR signaling in the castrate environment, and highlights new therapies either currently available or in clinical trials, including androgen synthesis inhibitors and novel direct AR inhibitors.
引用
收藏
页码：453 / +
页数：13
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