Cell-cycle dysregulation and the molecular mechanisms of prostate cancer

Prostate cancer is the most common cause of non-cutaneous cancer in men and although frequently latent is the second commonest cause of death. Screeni ng for the disease was historically based on symptoms of urethral obstructi on, clinical examination of the prostate gland and serum measurements of pr ostate specific antigen. As prostate cancer growth in the early stages is e nhanced by androgens, the mainstay of therapy has been androgen ablation by pharmaco-therapeutic or surgical means. The subsequent development of andr ogen therapy resistant prostate cancer in many patients, for whom therapeut ic options remain limited, has led researchers to focus attention on unders tanding the molecular genetics of prostate cancer. The array of genetic abn ormalities observed in prostate tumors, which include changes in components of the cell cycle, suggest the disease is quite heterogeneous and may requ ire further sub-classification based on genetic markers. Such analyses may lead to identification of relevant new prognostic and therapeutic indicator s. The advent of transgenic mouse models of prostate cancer may provide a c ritical tool for the implementation of rational genetic based therapeutics and alternate drug design.