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Prostate cancer is the second leading cause of cancer-related deaths in US men, primarily due to the development of castration-resistant (CR) prostate cancer (PCa), of which there are no effective treatment options. Reactive oxygen species (ROS) plays a critical role in prostate carcinogenesis, including the progression of the CR PCa phenotype. ROS regulates both cell proliferation and apoptosis; a moderate increase in ROS can promote proliferation; however, a substantial rise in ROS levels will result in apoptosis. Oxidase p66Shc is elevated in clinical PCa cells and has been associated with a metastatic phenotype of CR PCa cells, promoting PCa cell proliferation and migration in culture. However, ROS generated by p66Shc can also result in apoptosis. Our working hypothesis is that aberrant p66Shc/ROS production promotes PCa progression to the CR phenotype.