ABSTRACT
Neoplastic change in prostatic cells is not simply the result of a single mutational event, but rather a series of sequential interrelated mutations. The precise sequence of these events in prostatic neoplasia has yet to be elucidated, but a putative molecular scenario is depicted in Figure 24. Activation of the ras and c-erb B-2 oncogenes, and deletion of the p53 tumor suppressor gene, may occur in a stepwise fashion. These changes confer local growth potential on prostatic epithelium, but metastatic capacity awaits further mutations involving deletions of cell adhesion molecules such as E-cadherin and the ability to elaborate angiogenesis factors. The considerable time required for this sequential series of intracellular events to occur may account for the observation that prostate cancer very seldom develops in men below 40 years of age and usually presents clinically in men beyond middle age.
