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Correlation between proliferation, apoptosis, and angiogenesis in prostate carcinoma and their relation to androgen
H Matsushima1, T Goto, Y Hosaka
1Department of Urology, Tokyo Police Hospital, Japan.
Background:
Proliferation, apoptosis, and angiogenesis are essential for carcinogenesis. Little is known regarding the relation between proliferation, apoptosis, and angiogenesis in untreated prostate carcinoma as well as alterations associated with androgen ablation.
Methods:
Eighty patients who underwent radical prostatectomy for clinically localized prostate carcinoma were recruited for the study. The study population included 2 groups: 35 patients receiving 3-month neoadjuvant hormonal treatment using a combination of luteinizing hormone-releasing hormone analogue and the antiandrogen flutamide (NHT group) and 45 patients without prior treatment (non-NHT group). The authors measured the Ki-67 labeling index (Ki-67 LI) by MIB-1 immunohistochemistry, the apoptotic index (AI) by the terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling technique, and intratumoral microvessel density (IMVD) by CD31 immunohistochemistry on serial sections of formalin fixed, paraffin embedded tissues. Correlations among these parameters were examined in both groups.
Results:
A significant decrease in the Ki-67 LI coupled with a significant increase in AI was found in the NHT group compared with the non-NHT group, whereas IMVDs in both groups were not significantly different. AI was related to IMVD inversely in the non-NHT group (correlation coefficient [r] = -0.327; P = 0.03); in contrast, AI was related to IMVD positively in the non-NHT group (r = 0.579; P < 0.001). The Ki-67 LI was related to AI significantly in the non-NHT group but not in the NHT group. There was no correlation between Ki-67 LI and IMVD in either group.
Conclusions:
Correlations between proliferation, apoptosis, and angiogenesis in prostate carcinoma are altered significantly in association with androgen ablation. The results indicate that spontaneous apoptosis is suppressed by neovascularization, whereas hormone-induced apoptosis is enhanced in hypervascular tumors.