{"title":"原癌基因Bcl-2在慢性丙型肝炎病毒感染的肝癌肿瘤细胞中表达少","authors":"Yoshiki Ito , Norio Hayashi , Yutaka Sasaki , Masayoshi Horimoto , Shigeo Wada , Yuji Tanaka , Taizo Hijioka , Kunio Suzuki , Hideyuki Fusamoto , Jiro Fujimoto , Eizo Okamoto , Takenobu Kamada","doi":"10.1016/0928-4346(96)00263-0","DOIUrl":null,"url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":13746,"journal":{"name":"International Hepatology Communications","volume":"4 6","pages":"Pages 316-325"},"PeriodicalIF":0.0000,"publicationDate":"1996-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0928-4346(96)00263-0","citationCount":"4","resultStr":"{\"title\":\"Little expression of proto-oncogene Bcl-2 in tumourous cells of hepatocellular carcinoma with chronic hepatitis C virus infection\",\"authors\":\"Yoshiki Ito , Norio Hayashi , Yutaka Sasaki , Masayoshi Horimoto , Shigeo Wada , Yuji Tanaka , Taizo Hijioka , Kunio Suzuki , Hideyuki Fusamoto , Jiro Fujimoto , Eizo Okamoto , Takenobu Kamada\",\"doi\":\"10.1016/0928-4346(96)00263-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>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.</p></div>\",\"PeriodicalId\":13746,\"journal\":{\"name\":\"International Hepatology Communications\",\"volume\":\"4 6\",\"pages\":\"Pages 316-325\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0928-4346(96)00263-0\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Hepatology Communications\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0928434696002630\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Hepatology Communications","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0928434696002630","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Little expression of proto-oncogene Bcl-2 in tumourous cells of hepatocellular carcinoma with chronic hepatitis C virus infection
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.