Inactivation of tumour suppressor gene function is a critical step in the development of human neoplasia. The Rb and CDKN2 tumour suppressor genes are inactivated in many tumour types, including the late stages of prostate cancer, and appear to function in the same suppressor pathway. p53, another major tumour suppressor is also mutated in a subset of advanced-stage prostate carcinomas. E-cadherin and other cell adhesion genes, which have been characterized as suppressors of the metastatic phenotype, are inactivated or downregulated during progression to advanced prostate cancer and have been associated with poor clinical outcome. The early genetic events involved a prostatic neoplasia are poorly understood, but loss of as yet undiscovered tumour suppressor genes may play a role in the initiation of this disease.