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AIM To observe the roles of N-ras gene mutation and hepatitis B virus (HBV) infection in the carcinogenesis of hepatocellular carcinoma (HCC) in Guangxi, China.METHODS The polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and immunohistochemistry were used to detect N-ras gene mutation and HBV infection in 29 cases of HCC.RESULTS The aberration rates at codon 2-37 of N-ras were 79.31% in HCCs and 80.77% in adjacent non-tumorous liver tissues. More than 2 point mutations of N-ras gene were observed in 22 (75.86%) cases. HBsAg and HBxAg positive rates were 86.2% and 79.3%. There was a parallel tendency between HBV marker detections and the mutation rate of N-ras gene.CONCLUSION HBV infection and N-ras gene mutation may be involved in the carcinogenesis and development of HCC in Guangxi. Since the aflatoxin B1 contamination is one of risk factors for HCC in this area, it may contribute to the mutation of N-ras gene in carcinogenesis of HCC.INTRODUCTIONHepatocellular carcinoma (HCC) is one of common malignant tumors in People′s Republic of China. Guangxi is a high incidence area of HCC. Many factors are involved in hepatocarcinogenesis. Many studies revealed that hepatitis B virus (HBV) infection might be a risk factor for hepatocellular carcinogenesis. One theory for hepatocarcinogenesis is that the oncogene(s) may be transactivated by hepatitis B x antigen (HBxAg)[1]. It is found recently that activation of N-ras gene may be the molecular basis for the carcinogenesis and development of HCC[2,3]. There have been reports about overexpression of N-ras oncogene in human HCC[4], but a few dealt with the roles of N-ras gene mutation and HBV infection, and their relationship with HCC. We analyzed the N-ras gene mutation and HBV infection in HCC by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and immunohistochemistry in 29 cases of human HCC.