INTRODUCTION: While androgen deprivation therapy remains the primary treatment modality for patients with metastatic prostate cancer, treatment is uniformly marked by progression to castration resistant prostate cancer (CRPC). Abiraterone is the first new drug to enter clinical practice in a series of novel agents designed to potently target adrenal and tumor androgen production. MATERIALS AND METHODS: Herein, we review the mechanism of action of abiraterone and the phase III data supporting its approval for patients with metastatic CRPC. We discuss practical treatment considerations, including the incidence and management of side effect and monitoring requirements, and conclude by discussing future directions in the use of abiraterone, including early data supporting an expanded role for abiraterone in castration sensitive disease. RESULTS: Accumulating data emphasize that "androgen independent" or "hormone refractory" tumors remain sensitive to hormonal activation and suggest that despite suppression of circulating testosterone (T), residual tumor androgens play a prominent role in mediating CRPC progression. CONCLUSIONS: Accordingly, therapeutic strategies such abiraterone that more effectively target production of intratumoral androgens are necessary.
INTRODUCTION: While androgen deprivation therapy remains the primary treatment modality for patients with metastatic prostate cancer, treatment is uniformly marked by progression to castration resistant prostate cancer (CRPC). Abiraterone is the first new drug to enter clinical practice in a series of novel agents designed to potently target adrenal and tumor androgen production. MATERIALS AND METHODS: Herein, we review the mechanism of action of abiraterone and the phase III data supporting its approval for patients with metastatic CRPC. We discuss practical treatment considerations, including the incidence and management of side effect and monitoring requirements, and conclude by discussing future directions in the use of abiraterone, including early data supporting an expanded role for abiraterone in castration sensitive disease. RESULTS: Accumulating data emphasize that "androgen independent" or "hormone refractory" tumors remain sensitive to hormonal activation and suggest that despite suppression of circulating testosterone (T), residual tumor androgens play a prominent role in mediating CRPC progression. CONCLUSIONS: Accordingly, therapeutic strategies such abiraterone that more effectively target production of intratumoral androgens are necessary.
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