bcl-2 and bax Expression in Prostate Carcinoma

Song, Young Jun; Yang, Dae Yul; Lee, Sung Ho; Nam, Eun Sook; Kim, Sung Yong; Kim, Hayoung; Park, Heung Won

Abstract

PURPOSE: Proteins encoded by bcl-2 family as regulators of apoptosis appear to have significant cellular effects such that when abnormally expressed, they may render certain cells more susceptible to aberrant proliferation. The ratio of anti-apoptotic to pro-apoptotic bcl-2 family proteins appears to control the relative sensitivity or resistance of cells to apoptotic stimuli. The primary goal of this study is to determine the expression pattern of bcl-2 and bax in prostate carcinoma and to correlate them with Gleason score, T stage, and PSA to determine their prognostic potential.
MATERIALS AND METHODS
We examined the cellular expression of bcl-2 and bax proteins using immunohistochemical metod in a total 35 patients with untreated prostatic carcinoma. All tissues were scored for overall tissue expression as follows: bcl-2(0,<1%; 1+, 1-25%; 2+, 26-50%; 3+, >50%), bax(1+,<50%; 2+, 51-75%; 3+, >75%).
RESULTS
Of the 35 cases, 16(45.7%) contained at least 1% bcl-2 positive tumor cells. The bcl-2 positive cases included 1(7.7%) Gleason 2 to 4 grade tumors, 8(66.7%) Gleason 5 to 7 tumors, 7(70.0%) Gleason 8 to 10 tumors. bcl-2 protein expressed more frequently in higher grade(p<0.05) and in higher PSA level(p<0.05) of tumors. bax immunostaining was positive for all 35(100%) and 1+ was 16(45.7%), 2+ was 14(40.0%), 3+ was 5(14.3%). But statistically significant differences in bax expression among grade, T stage, and PSA were not observed. The bcl-2 protein was present mainly in the basal cells, but bax was in both basal and secretory cells of prostate.
CONCLUSIONS
bcl-2 protein have some potential role in progression of prostate carcinoma. Therefore, studies that evaluate the expression of these bcl-2 family genes in varoius time during progression of tumors correlate with the state of hormone dependency, response to therapy and duration of response are needed.