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Mounting evidence suggests that androgen-receptor activation and signaling underlie the pathology in patients with prostate cancer who have progressive disease despite having achieved low serum testosterone levels following androgen-deprivation therapy (i.e., castrate-resistant prostate cancer [CRPC]). In phase I and phase II trials of men who were chemotherapy naive and had CRPC, abiraterone acetate substantially lowered prostate-specific antigen (PSA) levels. The activity of this agent seems to result from potent, selective, and irreversible inhibition of CYP17, a key enzyme involved in androgen and estrogen synthesis.
To assess further the activity and tolerability of abiraterone acetate, investigators conducted an international phase II …