ABSTRACT
Androgen ablation is standard initial treatment for patients with metastatic prostate cancer. Though effective, patients invariably develop resistance and progress to a so-called ‘‘androgen-independent’’ state (1). These patients often respond to second-and third-line hormonal therapies, suggesting that their tumors remain dependent upon steroid receptor signaling. Molecular profiling studies of androgen-independent tumors suggest that androgen receptor (AR) reactivation is a common feature of prostate cancer progression following androgen withdrawal (2,3). These findings support the contention that most castration resistant prostate cancers remain AR-dependent.
