This chapter discusses the role of androgens in prostatic cancer. Prostatic cancer incidence increases with age more rapidly than any other type of cancer and less than 1% of prostatic cancers are diagnosed in men under 50 years of age. It is well established that the conversion of a normal cell to a fully malignant metastatic cancer cell involves a series of phenotypic changes. These phenotypic changes are themselves a result of a series of genetic changes in two basic classes of genes, oncogenes and tumor suppressor genes. Any alteration in the tightly regulated control of the expression of an oncogene can enhance the malignant phenotype of the cell. Qualitative changes involve genetic mutations in the oncogenes resulting in an altered oncogenic protein with a deregulated function. In prostatic cancer cells, loss of heterozygosity (LOH) for p53 can be coupled with a mutation that prevents any p53 protein from being produced. It is found that such a null mutation leads to complete loss of the p53 tumor suppressor function. Alternatively, LOH for p53 can be coupled with a mutation in the p53 gene that results in the expression of an alternative protein with positive oncogenic abilities.