| BACKGROUND & OBJECTIVE:Colorectal carcinoma (CRC) is a sort of common malignant tumor of digestive tract, but its pathogenesis has not been completely known. As can be seen from the angle of molecular biology, alterations of many genes are involved in colorectal carcinogenesis. Colorectal carcinoma includes heritage colorectal carcinoma and sporadic colorectal cancer (SCC).More than 80 percent cancers among colorectal carcinoma are SCC. Fragile histidine triad gene (FHIT) is considered a tumor suppressor gene which was found in recent years. It's reported that los of KTIT expression is perhaps frequent affair in human gastrointestinal tract carcinomas. Human mut S homolog2 (hMSH2) is a kind of human mismatch repair (hMMR) genes, hMMR genes are a set of human genes that are homologous with bacteria and yeast. They can repair the errors of DNA replication, which cannot only lead to frequent microsatellite instability, but also increase the mutations in some pro-oncogenes and suppressor genes. Therefore the mutations of hMMR genes can induce tumorigenesis. Recent studies have suggested that FHIT inactivation can be a consequence of defects in hMSH2.But the researchs of FHIT, hMSH2 and their correlation with the carcinogenesis and progression of SCC are few. This study was designed to investigate the expression and clinic significance of FHIT and hMSH2 protein in human SCC. Materials and method:70 cases of SCC samples, 24 cases of adenoma and 14cases normal mucosa samples were collected. All tissues were identified by pathologist. Immunohisochemical streptavidin peroxides conjugate method was used to analyze the expression of FHIT, as well as hMSH2, in normal colorectal mucoma, colorectal adenoma and colorectal carcinoma. All the dates were analyzed by SPSS10.0 statistical package, The Chi-square test and fisher'... |