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.
Written by:
Friedlander TW, Ryan CJ. Are you the author?
Division of Genitourinary Medical Oncology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA.
Reference: Urol Clin North Am. 2012 Nov;39(4):453-64.
doi: 10.1016/j.ucl.2012.07.003
PubMed Abstract
PMID: 23084523
UroToday.com Investigative Urology Section