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Role of hepatitis B virus base core and precore/core promoter mutations on hepatocellular carcinoma in untreated older genotype C Chinese patients
Author(s) -
Zheng JX.,
Zeng Z.,
Zheng Y. Y.,
Yin SJ.,
Zhang DY.,
Yu YY.,
Wang F.
Publication year - 2011
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2011.01458.x
Subject(s) - hepatocellular carcinoma , hepatitis b virus , medicine , genotype , virology , hbeag , mutation , virus , biology , gene , genetics , hbsag
Summary. The aim of the study was to investigate the prevalence of mutations of basal core promoter (BCP) and precore (PreC) region of hepatitis B virus (HBV) and their association with hepatocellular carcinoma. A total of 341 untreated older HBV patients were divided into three groups: chronic hepatitis B (CHB, 185), cirrhotic hepatocellular carcinoma (LC‐HCC, 113) and non‐cirrhotic hepatocellular carcinoma (non‐LC‐HCC, 43). HBV BCP and PreC mutations and genotypes were determined by direct sequencing. Using univariate analysis, age (≥45 years), single mutations including A1896 and A1899 and multiple mutations T1762/A1764 + A1896, T1762/A1764 + A1899 and T1762/A1764 + A1896 + A1899 were more frequently detected in LC‐HCC and non‐LC‐HCC patients than in CHB patients. BCP T1762/A1764 mutations were highly detected in LC‐HCC patients than in CHB patients. Multivariate logistic regression analysis (adjusted for age and gender) revealed that among HBeAg‐positive patients, BCP T1762/A1764 mutations (OR, 5.975; P = 0.05), PreC A1899 mutation (OR, 4.180; P = 0.013) and multiple mutations T1762/A1764 + A1899 (OR, 6.408; P = 0.006) were independently associated with the development of LC‐HCC; PreC A1899 mutation (OR, 7.347; P = 0.034) was also independently associated with the development of non‐LC‐HCC. On the other hand, among HBeAg‐negative patients, PreC A1896 mutation (OR, 5.176; P = 0.002) and multiple mutations T1762/A1764 + A1896 (OR, 4.149; P = 0.007) were independently associated with the development of non‐LC‐HCC. These results indicated that older age (≥45 years) was associated with LC‐HCC and non‐LC‐HCC development. BCP T1762/A1764 mutations and PreC A1899 mutation were associated with the LC‐HCC development in HBeAg‐positive patients. PreC A1896 mutation was associated with the non‐LC‐HCC development in HBeAg‐negative patients.