Molecular and cellular changes associated with the acquisition of metastatic ability by prostatic cancer cells.

Presently, one of every four cancers diagnosed in American males is of prostatic origin. Once prostatic cancer metastasizes, it is a fatal disease for which no therapy presently available is curative. Because of these facts, there is a growing interest in the early detection and screening of men for prostate cancer. Such screening could potentially identify 10 million American men with histological prostatic cancer. It is estimated that approximately 7% (700,000) of these men will eventually die from their disease if left untreated. This raises the critical question of which of the remaining 93% (9,300,000) of men with nonlethal, but potentially life-altering, histologically detectable prostatic cancer should receive therapy. There is no diagnostic method presently available which allows men with histologically detectable prostatic cancer, who require immediate therapy, to be distinguished from those requiring either delayed therapy or no treatment. Acquisition of metastatic ability by such histologically detectable prostatic cancer cells is a definitive criterion upon which to base such a diagnostic substaging method. Identification of the cellular and molecular requirements for acquisition of metastatic ability by prostatic cancer cells is needed for the development of such methods. This article will focus on what is known concerning general cellular and specific molecular changes associated with the acquisition of metastatic ability by prostatic cancer cells, and suggested areas for future studies.