The activation of oncogenes and inactivation of tumor suppressor genes (TSGs) have been implicated in the development of many human and animal malignancies. Changes in certain specific genes have been shown to be of potential value for diagnosis and prognosis, as well as treatment, of some cancers. By contrast, no oncogene has been correlated conclusively at the DNA level with the initiation and progression of prostate cancer, although though there are alterations in expression of a number of oncogenes (i.e., ras, c-sis, c-fos, and neu) in messenger RNA and/or protein level. It is also thought that alterations of certain known TSGs, such as p53, KAII, and E-cadherin, may be important in prostate carcinogenesis; alterations of KAII (known as a metastasis suppressor gene) and p53 are more likely to be associated with the late events in the development of prostate cancers. Other TSGs, such as Rb, nm23, and PACI, require more studies to further define their role. The possible presence of TSGs in frequently altered regions on chromosomes 6q14-21, 8q, 10p, 10q, 13q, and 17p have been actively studied. Moreover, further studies on other frequently altered regions on chromosomes 2q, 5q, 15q, 16q, l7q, and 18q may provide further insight into the mechanism of prostate cancer progression. Future studies should be targeted on these putative oncogenes and TSGs and to determine whether assessment of specific gains or losses may have prognostic value in the diagnosis and treatment of prostate cancer.