The incidence of human prostate cancer has been continuously increasing during the last decade to such a point that prostatic carcinoma has become the most prevalent neoplasm and the second principal cause of cancer death in men.’The shortage of suitable tools for either screening or early diagnosis as well as the limited knowledge on both the etiology and the regulation of development and growth of the prostate tumor burden this cancer with an unfavorable prognosis and leave clinicians at a loss in the management of patients. In the past decades, several obstacles have critically obstructed prostate cancer studies. In the first place, the potential use of androgen receptors (AR) both as prognostic indicators and as predictors of response of patients to endocrine treatment has been hampered either by methodological pitfalls in the receptor assays or by the heterogeneous composition of most tumor tissues: the situation is further complicated by developmental and functional features inherent in the human prostate gland that make it highly heterogeneous in nature. Second, little is known on the mechanisms whereby such tumor types invariably tend to progress from an endocrine towards a hormone-refractory status. Finally, insensitivity of androgenindependent tumor growth to endocrine maneuvers is also reflected in the failure of androgen ablation to induce programmed cell death, as conversely occurs in hormone-dependent prostatic tumors or normal prostate. Androgens are thought to be necessary for prostate development and maintenance of both cell number and functional activity in the adult gland. It is universally recognized that the conversion of circulating testosterone into its biologically