Proliferative and apoptotic activities, as well as p53 protein expression, of ten untreated primary prostate carcinomas that showed extremely poor response to hormonal therapy (primary androgen independent prostate carcinomas) were compared with the stage- and grade-matched primary tumor specimens with favorable response to hormonal therapy (androgen dependent prostate carcinomas). The mean proliferative activity measured by Ki-67 immunohistochemistry was slightly higher in the primary androgen independent prostate carcinomas (8.70+/-5.24) than in the androgen dependent prostate carcinomas (7.09+/-2.68; p=0.27). The mean apoptotic activity by in situ end-labeling technique in the primary androgen independent prostate carcinomas (0.96+/-1.03) was less than half of that in the androgen dependent prostate carcinomas (2.75+/-0.98; p=0.0001). Ten percent of the androgen dependent prostate tumors showed p53 protein expression, whereas 30% of the primary androgen independent prostate tumors were immunopositive for p53 (p=0.30). In summary, we have shown that apoptotic activity in the primary androgen independent prostate carcinomas is significantly lower than in the matched androgen dependent prostate carcinomas while the proliferative activity remains unaffected. These results suggest that primary androgen independent prostate carcinomas may have genetic properties, such as inactivation of the p53 gene, that enable them to escape apoptosis caused by androgen ablation.