(Background) The anti-androgen therapy usually used to manage prostatic cancer is effective because the growth of adenocarcinoma of the prostate is influenced by androgens. However, some prostatic cancers do not respound to hormone therapy. Many studies have been conducted with the objective being to assess the responsiveness of prostatic cancer tissues by measuring the amount of androgen receptors (AR). The present study investigates the expression of AR in adenocarcinoma and in benign adenoma of the human prostate.
(Methods) Formaline fixed paraffin sections of adenocarcinoma were prepared using 86 patients with primary prostatic cancer, seven patients with relapsed prostatic cancer, and 26 patients with BPH (as the control). Specimens were obtained by needle biopsy and immunohistochemical staining was performed.
(Results) The benign adenoma AR were stained in the nuclei of the glandular epithelial cells. The receptor-positive and receptor-negative cells were intermingled with the malignant prostatic cells. The labelling indexes (LI) of the androgen receptor stain values in adenocarcinoma of the prostate (57.8±14.5%) in 86 patients were significantly lower than benign adenoma (86.4±6.3%) (p=0.0001). And the LI were decreased with the progress of grades in malignancy: 72.8±7.5% in well defferanciated; 58.7±7.3% in moderately differanciated; and 41.4±8.2% in poorly differanciated adenocarcinoma (p=0.0001). Moreover, LI in relapsed case, all of which were poorly differanciated (22.9±13.6%), were significantly lower than the LI values of the primary cancer cases with poorly differanciated adenocarcinoma (p=0.0004). Responders to anti-androgen therapy had high AR positive rate (p=0.0001) and weakly stained cases had a lower survival rate than strongly stained cases (p=0.03).
(Conclusion) These results suggest that the detection of AR with immunohistochemical study is useful for estimating the prognosis of the patients undergone anti-androgen therapy. And prostatic cancer cells are heterogenously composed of clones of both androgen dependent and independent cancer cells before hormonal therapy is begun. And one reason why these tumors easily relapse with the progress of grades in hormonal therapy.