Premium
Expression of the Apoptosis suppressing protein bcl‐2 in prostatic adenocarcinoma is related to tumor malignancy
Author(s) -
Lipponen P.,
Vesalainen S.
Publication year - 1997
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19970615)32:1<9::aid-pros2>3.0.co;2-i
Subject(s) - immunohistochemistry , malignancy , adenocarcinoma , prostate , pathology , prostate cancer , medicine , apoptosis , cancer research , cancer , biology , biochemistry
BACKGROUND The expression of bcl‐2 protein has been related to histopathological features and prognosis in several epithelial tumors. In prostatic adenocarcinoma the prognostic significance of bcl‐2 expression is mainly unexplored. METHODS The expression of bcl‐2 protein was assessed in 235 prostatic adenocarcinomas by using monoclonal bcl‐2 protein antibody after microwave pretreatment of the cancer sections. The results of immunohistochemistry were related to histopathological features and prognosis of the patients. RESULTS 71% of the tumors were bcl‐2 negative, in 18% of cases the expression was weak, and in 11% of cases strong. The fraction of bcl‐2 positive cells was variable (mean [SE]: 15 [2]%). The expression of bcl‐2 protein was positively correlated to high T‐category, metastatic disease, and poor histological differentiation of the tumor. Tumors that were aneuploid and rapidly proliferating frequently expressed bcl‐2 protein, while tumors we densely infiltrated by inflammatory cells rarely expressed bcl‐2. The expression of bcl‐2 protein was related to lowered survival probability in univariate analysis, while in multivariate analysis the expression of bcl‐2 had no independent prognostic value. CONCLUSIONS The expression of bcl‐2 protein in prostatic adenocarcinoma is related to tumor malignancy, but the prognostic significance of the expression requires further analyses, particularly in localized tumors. Prostate 32:9–15, 1997. © 1997 Wiley‐Liss, Inc.