Prostatic adenocarcinoma is emerging as a major cause of morbidity and
mortality in the male population in the western world. Programmed cel
l death (apoptosis) in the prostate is activated by hormone ablation a
nd is under the control of several regulating genes including the tumo
ur suppressor gene p53 and the proto-oncogene bcl-2. Bcl-2 belongs to
a rapidly expanding family of genes which form two functionally antago
nistic groups controlling cell death and survival. Apoptosis regulatin
g genes appear to play an important role in the development and progre
ssion of prostatic adenocarcinoma and offer a potential target for fut
ure therapeutic strategies.