Abstract
In the last few years, there has been a rekindled interest in the androgen receptor (AR) and AR signaling as valid therapeutic targets in prostate cancer. While the primary goal of therapy for recurrent or advanced prostate cancer has long been to reduce circulating and intratumoral androgen levels, recent laboratory and clinical data have shown that AR signaling remains active (and continues to drive tumor growth) even in the castration-resistant state (1).
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