|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1764A |
|
Mutation Site Sentence
|
Statistically significant summary odds ratios of HCC were obtained for any PreS mutation (3.77, 95% confidence interval [CI] = 2.57 to 5.52), C1653T in EnhII (2.76, 95% CI = 2.09 to 3.64), T1753V (2.35, 95% CI = 1.63 to 3.40), and A1762T/G1764A in BCP (3.79, 95% CI = 2.71 to 5.29). |
|
Mutation Level
|
Nucleotide level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
BCP |
|
Standardized Encoding Gene
|
|
|
Genotype/Subtype
|
D;B2;B;C1;C2;F;C;A |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Hepatitis B Virus Infection
Carcinoma, Hepatocellular
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
- |
|
Location
|
- |
|
Literature Information
|
|
PMID
|
19574418
|
|
Title
|
Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis
|
|
Author
|
Liu S,Zhang H,Gu C,Yin J,He Y,Xie J,Cao G
|
|
Journal
|
Journal of the National Cancer Institute
|
|
Journal Info
|
2009 Aug 5;101(15):1066-82
|
|
Abstract
|
BACKGROUND: The association between hepatitis B virus (HBV) mutations and hepatocarcinogenesis remains controversial because of conflicting data in the literature. We conducted a meta-analysis of case-control and cohort studies to examine HBV PreS, enhancer II (EnhII), basal core promoter (BCP), and precore mutations in relation to the risk of hepatocellular carcinoma (HCC). METHODS: We searched databases for studies of these associations that were published in English or Chinese up to August 31, 2008. HBV mutation-specific odds ratios and relative risks were pooled by use of a random-effects model and stratified by potential confounders. All statistical tests were two-sided. RESULTS: Of the 43 studies included in this meta-analysis, 40 used a case-control design. The 43 studies evaluated a total of 11 582 HBV-infected participants, of whom 2801 had HCC. Statistically significant summary odds ratios of HCC were obtained for any PreS mutation (3.77, 95% confidence interval [CI] = 2.57 to 5.52), C1653T in EnhII (2.76, 95% CI = 2.09 to 3.64), T1753V (2.35, 95% CI = 1.63 to 3.40), and A1762T/G1764A in BCP (3.79, 95% CI = 2.71 to 5.29). PreS mutations were more strongly associated with an increased risk of HCC in subjects who were infected with HBV genotype C than in those who were infected with HBV genotype B, whereas the opposite was true for A1762T/G1764A. C1653T, T1753V, and A1762T/G1764A were more strongly associated with an increased risk of HCC in hepatitis B e antigen (HBeAg)-positive subjects than in HBeAg-negative subjects. PreS mutations, C1653T, T1753V, and A1762T/G1764A accumulated during the progression of chronic HBV infection from the asymptomatic carrier state to HCC (P(trend) < .001 for each mutation). PreS mutations, C1653T, C1653T + T1753V, and A1762T/G1764A-based combinations of mutations had specificities greater than 80% for the prediction of HCC. The precore mutations G1896A and C1858T were not associated with the risk of HCC, regardless of HBeAg status and HBV genotype. CONCLUSIONS: HBV PreS mutations, C1653T, T1753V, and A1762T/G1764A are associated with an increased risk of HCC. These mutations alone and in combination may be predictive for hepatocarcinogenesis.
|
|
Sequence Data
|
AB241109-AB241117;AB307808-AB307967
|
|
|