Prostate cancer is the most common non-skin cancer in America, affecting 1 in 7 men. While better screening and treatment have resulted in improved outcomes, a subset of patients eventually develops metastatic disease. Androgen deprivation therapy is initially effective, but incurable castration-resistant prostate cancer inevitably develops. While the new generation of anti-androgen therapies has shown promise, survival improvements have been measured in months. How prostate cancer cells acquire the ability to survive and proliferate after androgen deprivation therapy remains to be determined. Importantly, the failure of androgen deprivation therapy is not accompanied by the loss of androgen receptor (AR) or AR activity, but rather with restored AR activation through a variety of mechanisms. The focus of our research has been on elucidating AR-mediated gene expression and how AR signaling cross talks with other signaling pathways in prostate cancer, such as WNT signaling and DNA repair pathway. The goal of our research is to understand the mechanisms that lead to prostate cancer development and progression and translate that mechanistic understanding into therapeutics to prevent, delay and treat the disease.