Growth Regulatory Networks in the Prostate

Abstract

Fifty years ago, Huggins and his colleagues [1,2] established that prostate carcinoma could respond to castration or oestrogen therapy, thereby inaugurating a form of treatment which has not been superseded. This unfortunately is not a reflection of the effectiveness or success of antiandrogen therapy: although most men with metastatic prostate cancer treated with some form of androgen withdrawal therapy show an initial beneficial response of no mean palliative value [3], an almost inevitable relapse of the disease to an androgen-insensitive state leads to death from the progressive cancer [4]. In short, in the last half-century, the annual death rate from prostate cancer has not decreased, and it remains a fatal disease for which no therapy increases survival [5]. Also, as increasing age is the most distinctive or identifiable factor associated with the incidence of prostatic cancer, the improving longevity of Western European and North American male populations will increase the number of sufferers and will continually exacerbate the burden placed on the health services in terms of man-hours and on private or state-borne medical costs [6,7].