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Basic Characteristics of Mutations
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Mutation Site
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G1896A |
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Mutation Site Sentence
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BACKGROUND AND OBJECTIVE: Precore (PC) variant (G1896A) and basal core promoter (BCP) variant (A1762T/G1764A) of HBV are associated with risk of hepatocellular carcinoma in HBV carriers. |
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Mutation Level
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Nucleotide level |
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Mutation Type
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Nonsense mutation |
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Gene/Protein/Region
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PreC |
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Standardized Encoding Gene
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C
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Genotype/Subtype
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B;C |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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Carcinoma, Hepatocellular
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Immune
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- |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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Y |
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Treatment
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- |
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Location
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China |
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Literature Information
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PMID
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24763132
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Title
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Higher proportion of viral basal core promoter mutant increases the risk of liver cirrhosis in hepatitis B carriers
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Author
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Tseng TC,Liu CJ,Yang HC,Chen CL,Yang WT,Tsai CS,Kuo SF,Verbree FC,Su TH,Wang CC,Liu CH,Chen PJ,Chen DS,Kao JH
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Journal
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Gut
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Journal Info
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2015 Feb;64(2):292-302
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Abstract
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BACKGROUND AND OBJECTIVE: Precore (PC) variant (G1896A) and basal core promoter (BCP) variant (A1762T/G1764A) of HBV are associated with risk of hepatocellular carcinoma in HBV carriers. However, little is known about their impact on the adverse outcomes of hepatitis B e antigen (HBeAg)-negative hepatitis and liver cirrhosis. METHODS: 251 spontaneous HBeAg seroconverters who had genotype B or C infection and received a long-term follow-up were enrolled. PC and BCP mutants were determined qualitatively and quantitatively to correlate with these adverse outcomes. The findings were validated by an independent case-control study, which included 184 patients with biopsy-proven liver fibrosis stages. RESULTS: In the longitudinal cohort study, BCP mutant and possibly PC wild type were associated with cirrhosis development, but not HBeAg-negative hepatitis. Multivariable analysis showed that only BCP mutant was an independent risk factor for cirrhosis development. Using quantitative analysis of BCP mutant, a higher proportion of BCP mutant, defined as a continuous variable, a dichotomous variable or an ordinal variable, was associated with a higher risk of cirrhosis. If we chose 45% of BCP mutant as the cut-off, the risk of cirrhosis was higher in patients with BCP mutant >/=45% compared to <45% in the longitudinal cohort; this finding was validated by the case-control study (adjusted OR: 2.81, 95% CI 1.40 to 5.67). CONCLUSIONS: A higher proportion of BCP mutant increases the risk of liver cirrhosis development in HBV carriers with genotype B or C infection.
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Sequence Data
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-
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