Prostate cancer progression after androgen deprivation therapy: mechanisms of castrate resistance and novel therapeutic approaches.
Prostate cancer progression after androgen deprivation therapy: mechanisms of castrate resistance and novel therapeutic approaches.
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Prostate cancer is the second-leading cause of cancer-related mortality in men in Western societies. Androgen receptor (AR) signaling is a critical survival pathway for prostate cancer cells, and androgen-deprivation therapy (ADT) remains the principal treatment for patients with locally advanced and metastatic disease. While a majority of patients initially respond to ADT, most will eventually develop castrate-resistance, defined as disease progression despite serum testosterone levels of less than 20ng/dL. The recent discovery that AR signaling persists during systemic castration via intratumoral production of androgens led to the development of novel anti-androgen therapies including abiraterone acetate and enzalutamide. While these agents effectively palliate symptoms and prolong life, metastatic castration-resistant prostate cancer (mCRPC) remains incurable. An increased understanding of the mechanisms that underlie the pathogenesis of castrate-resistance is therefore needed to develop novel therapeutic approaches for this disease. The aim of this review is to summarize the current literature on the biology and treatment of castrate-resistant prostate cancer.
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