- 现金
- 62111 元
- 精华
- 26
- 帖子
- 30441
- 注册时间
- 2009-10-5
- 最后登录
- 2022-12-28
|
<http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2893.2011.01458.x/abstract>
乙肝病毒的作用基地的核心和前C/核心启动子突变对
疗未经治的肝癌病人中老年人C基因型
Role of hepatitis B virus base core and precore/core promoter mutations on
hepatocellular carcinoma in untreated older genotype C Chinese patients
J-X. Zheng, Z. Zeng, Y. Y. Zheng, S-J. Yin, D-Y. Zhang, Y-Y. Yu, F. Wang
Article first published online: 4 APR 2011
DOI: 10.1111/j.1365-2893.2011.01458.x
© 2011 Blackwell Publishing Ltd
Issue
Journal of Viral Hepatitis
Early View (Online Version of Record published before inclusion in an
issue)
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. |
|