AR and posterior cortical atrophy: By using androgen-independent, androgen-receptor negative PC3 [23–24] and androgen-receptor positive 22Rv1 [25] PCa cell lines stable infected with shRNA for cyclin D1, we show that cyclin D1 is a key regulator in controlling the DNA double strand break (DSB) repair mechanisms mediated by the non homologous end joining (NHEJ) pathway and that the silencing cyclin D1 radiosensitizes PCa cells.