Friedlander Terence W, Ryan Charles J
Helen Diller Family Comprehensive Cancer Center, University of California-San Francisco, 1600 Divisadero Street, San Francisco, CA 94115, USA.
Curr Oncol Rep. 2009 May;11(3):227-34. doi: 10.1007/s11912-009-0032-4.
It is well recognized that the vast majority of prostate cancers rely on activation of the androgen receptor (AR) by circulating androgens for growth and survival. Three proven hormonal strategies to impair AR signaling are decreasing gonadal hormone production, inhibiting androgen-AR interaction, and impairing extragonadal androgen synthesis. In this review, we discuss the current strategies to slow initial and castration-resistant tumor growth through the use of hormonal agents such as the gonadotropin-releasing hormone analogues, antiandrogens, and adrenolytic agents, focusing on defining the optimal timing, combinations, and use of these agents, as well as on novel drug development.