The decades-old terminology of androgen independence has been replaced in recent years with castration-resistant prostate cancer.
Biological and clinical evidence have together conspired to support the use of this revised terminology by demonstrating that in the vast majority of cases tumors are neither truly depleted of androgens, nor are they free of the requirement for androgens to sustain growth and progression. Abiraterone acetate, an androgen synthesis inhibitor, and enzalutamide, a potent androgen receptor antagonist, both exploit the continued requirement for androgens. A central question, given the therapeutic gains enabled by further suppression of the androgen axis with these newer agents, is whether there may be additional clinical benefit gained by moving the goal posts of androgen suppression even further. The answer lies in part with the mechanisms utilized by tumors that enable resistance to these therapies. The aims of this review were to give a broad outline of steroidogenesis in prostate cancer and to highlight recent developments in understanding resistance to hormonal therapies.
Sharifi N. Are you the author?
Department of Cancer Biology, Lerner Research Institute, Glickman Urological and Kidney Institute and Taussig Cancer Institute, Cleveland Clinic, Ohio 44195.
Reference: Mol Endocrinol. 2013 May;27(5):708-14.