Objective To investigate the relationship between hepatitis B virus (HBV) genotype,the mutation in basic core promoter(BCP)region/pre-core(Pre-C)region and the incidence of hepatocellular carcinoma(HCC) in Fusui county of Guangxi Zhuang Autonomous Region (Guangxi),a area with high incidence of HCC. Methods In this case-control study,53 HCC patients and 70 asymptomatic HBV carriers were enrolled. Blood samples were collected from them for serum separation and HBV DNA extraction. The DNA sequences of the S region and BCP/Pre-C region of HBV was determined by direct sequencing following nested-PCR amplification. The relationship between the genotype,gene mutation of HBV and the incidence of HCC was analyzed. Results The mutation rates of the A1762T/G1764A in the BCP region and the T1858C in the Pre-C region of HBV were significantly higher in HCC group than in control group(94.3%vs. 75.7%,P=0.006;50.9%vs. 31.4%,P=0.029). The mutation rate of A1775G was significantly higher in control group (28.6%) than in HCC group (13.2%)(P=0.041). Multiple logistic regression analysis indicated that A1762T/G1764A and T1858C mutations are the risk factors for the development of HCC (OR=5.459,95%CI:1.397- 21.332,P=0.015;OR=3.881,95%CI:1.462-10.305,P=0.006). A1775G is the protective factor in the development of HCC(OR=0.192,95%CI:0.059-0.622,P=0.006). Conclusion The present investigation showed that BCP A1762T/G1764A,A1775G and Pre-C T1858C mutations are correlated with the incidence of HCC in Fusui county of Guangxi.

OBJECTIVETo identify specific serum glycoprotein profiles that correspond to the carcinogenic process of primary liver cancer (PLC) by analyzing a population with high-incidence of PLC using lectin affinity microarray.

METHODSSerum samples were collected from individuals classified as high risk for PLC (including patients with liver cirrhosis and hepatitis B) and development of PLC was recorded. Healthy individuals served as normal controls. The serum samples were subjected to glycoprotein profling by using lectin microarrays and the results were confirmed by lectin blot. Between-group differences were statistically analyzed.

RESULTSPLC carcinogenesis was found to be correlated with enhanced affinity for AAL, ACL, ConA, LCA, MPL, NML, PHA-E, PHA-L, PSA, RCA-I, STL, VAL,WGA, and SNA (P less than 0.05). These data implied that changes in specific glycan structures, such as aFuc, GlcNAc, GalNAc, mannose, bisecting GlcNAc and terminal beta1-4 Gal, may be involved in PLC carcinogenesis . The PLC group showed significantly different results for all detected lectins, except SNA (P less than 0.05). However, among the PLC group, the SNA affinity was not significantly different for the hepatitis B group (P =0.443, P more than 0.05).

CONCLUSIONGlycans may be associated with the carcinogenic process of PLC and may be developed as diagnostic and prognostic biomarkers of PLC in the future.

Carcinogenesis ; Chromatography, Affinity ; Cohort Studies ; Glycoproteins ; blood ; Humans ; Lectins ; blood ; Liver Neoplasms ; blood ; pathology

OBJECTIVETo investigate the relationship between hepatitis B virus (HBV) genotype, the mutation in basic core promoter (BCP) region/pre-core (Pre-C) region and the incidence of hepatocellular carcinoma (HCC) in Fusui county of Guangxi Zhuang Autonomous Region (Guangxi), a area with high incidence of HCC.

METHODSIn this case-control study, 53 HCC patients and 70 asymptomatic HBV carriers were enrolled. Blood samples were collected from them for serum separation and HBV DNA extraction. The DNA sequences of the S region and BCP/Pre-C region of HBV was determined by direct sequencing following nested-PCR amplification. The relationship between the genotype, gene mutation of HBV and the incidence of HCC was analyzed.

RESULTSThe mutation rates of the A1762T/G1764A in the BCP region and the T1858C in the Pre-C region of HBV were significantly higher in HCC group than in control group (94.3% vs. 75.7%, P = 0.006; 50.9% vs. 31.4%, P = 0.029). The mutation rate of A1775G was significantly higher in control group (28.6%) than in HCC group (13.2%) (P = 0.041). Multiple logistic regression analysis indicated that A1762T/G1764A and T1858C mutations are the risk factors for the development of HCC (OR = 5.459, 95% CI: 1.397-21.332, P = 0.015; OR = 3.881, 95% CI: 1.462-10.305, P = 0.006). A1775G is the protective factor in the development of HCC (OR = 0.192, 95% CI: 0.059-0.622, P = 0.006).

CONCLUSIONThe present investigation showed that BCP A1762T/G1764A, A1775G and Pre-C T1858C mutations are correlated with the incidence of HCC in Fusui county of Guangxi.

Carcinoma, Hepatocellular ; epidemiology ; virology ; Case-Control Studies ; China ; epidemiology ; DNA, Viral ; Genotype ; Hepatitis B virus ; genetics ; Humans ; Incidence ; Liver Neoplasms ; epidemiology ; virology ; Mutation ; Polymerase Chain Reaction ; Risk Factors ; Sequence Analysis, DNA