ABSTRACT
Prostate cancer remains the most common nonskin cancer and the second leading cause of cancer deaths in North American men. Patients with disease localized to the prostate gland can be cured by surgery and/or radiation therapy. Patients with metastatic disease currently cannot be cured and receive androgen deprivation therapy in palliative intent. This therapy encompasses castration, antiandrogen therapy, and combinations thereof (1,2). Androgen deprivation therapy causes a substantial regression of tumor burden in most patients, but ultimately fails due to the outgrowth of ‘‘hormone-refractory’’ cancer cells. Understanding the molecular mechanisms of tumor progression during androgen deprivation therapy is prerequisite to develop therapies against this lethal form of prostate cancer.
