Abstract
Abstract The proto-oncogene bcl-2, which was first found overexpressed in human follicular lymphoma, is now considered to inhibit apoptotic cell death, resulting in greater cell susceptibility to genetic alteration. Thus, this gene might cause hyperplasia or occasionally lead to a more malignant phase, i.e. carcinoma. Overexpression of this gene has been reported in several tumors. However, little has been clarified about its contribution to hepatocarcinogenesis. In this study, using immunoblotting, immunohistochemical and in situ hybridization techniques, we examined the expression of the bcl-2 protein and messenger RNA in patients having hepatocellular carcinoma with chronic hepatitis C virus infection. Immunoblot analysis indicated no significant differences in the amounts of bcl-2 protein between tumorous and nontumorous lesions. Furthermore, immunohistochemistry as well as in situ hybridization technique demonstrated that only lymphocytes infiltrating the tissues and tumors were bcl-2 positive. These findings suggest that the proto-oncogene bcl-2 may make no or little contribution, if any, to hepatocarcinogenesis.
Published Version
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