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“Background Prostate cancer (PC) has become the most prevalent malignant tumour in men in the Western World Axenfeld syndrome and the second leading cause of male cancer-related death. Initially, most tumours present androgen-sensitive carcinomas but the proportion of undifferentiated histology becomes more apparent when correlated to clinical progression and the development of hormone resistance occurrence [1, 2]. The explanation of the conversion of a hormone-sensitive status to a hormone-insensitive one is currently one of the most critical areas of debate in prostate carcinoma. Prostate specific antigen (PSA) is at present the better pre-treatment predictor of the disease and of its outcome after treatment. However, its sensitivity and specificity are not yet sufficient to make it the perfect screening test for prostate cancer. Prostate tumour is composed of a heterogeneous population of cells with different levels of androgen dependency. A decline in serum PSA does not always indicate a cure of cancer, as PSA production is androgen dependent and as a result the dedifferentiation of neoplastic cells gradually lose their capacity to produce PSA. Consequently, serum PSA is less reliable as a tumour marker in patients with high tumour grades and in hormonally treated patients with disseminated disease.