Biological basis for chemohormonal therapy for prostatic cancer

Abstract

Since the pioneering studies of Charles Huggins in the 1940s, androgen ablation therapy has been the standard treatment for metastatic prostatic cancer. This is because nearly all men with metastatic prostatic cancer have an initial, often dramatic, beneficial response to this hormonal therapy. This initial response demonstrates that at least a portion of the cancer cells are androgen responsive. While this initial response is of substantial palliative value, unfortunately, essentially all treated patients eventually relapse to an androgen-insensitive state and succumb to the progression of their cancer; cures, if any, are rare [1]. Because of this nearly universal relapse phenomenon, the annual death rate from prostatic cancer has not decreased at all over the subsequent 40 years since hormonal therapy became standard therapy [2]. In fact, over the last 40 years, the superficially benign nature of androgen ablation therapy has tended to disguise the fact that prostatic cancer is still a fatal disease for which no effective therapy is presently available [3]. This does not mean that hormonal therapy is not useful in the treatment of metastatic prostatic cancer, only that such hormonal therapy will have been used in combination with additional forms of therapy if the cure rate for metastatic prostatic cancer is ever going to be substantially increased.