Progression Model of Prostate Cancer

Prostate cancer is the most common form of cancer diagnosed in men (other than skin cancer). In 1999, in the United States alone there were approximately 179,300 new cases and 37,000 deaths due to prostate cancer (1 ). In 1999, the prostate cancers diagnosed accounted for 29% of cancers in men and 14.7% of all cancers (other than skin) in both sexes, making it the most diagnosed cancer in the total population. In the prostate, the formation of histologically identifiable neoplastic lesions is a very frequent event, occurring in nearly one-third of the male population over 45 years of age (2 ). Fortunately, it has been estimated that only a small percentage of these men will actually die from prostate cancer (3 –6 ). There is evidence to support environmental (including cell-cell interactions), epigenetic, and other factors playing a role in prostate tumorigenesis (7 –17 ). However, that cancer in general is a genetic disease is currently the most widely accepted model of tumor etiology (18 ,19 ). A number of genetic changes have been documented in prostate cancer. Consistently, allelic losses of specific chromosomes are observed in prostate tumors, but this is not true for mutations on specific genes (20 –22 ). Prostate cancers require many years to develop. It is believed that during these years they accumulate a number of genetic alterations. However, the molecular events that underlie the development of prostate neoplasia are not well defined (22 ). Thus, it has been difficult to establish a genetic model for the progression of prostate cancer.