Introduction: HBV mutations, including A1762T/G1764A, C1653T, T1753V, and T1674G/C, in the core promoter (CP) region of the viral genome are typically the ones that increase the risk of HCC.
Molecular characterization of hepatitis B virus in Vietnam.
Method: Mutations in the BCP (C1653T, T1674C/G, T1753 V, A1762T, G1764/A, C1766T, and T1768A) and the PC/core region (G1899A, C2002T, A2159G, A2189C, and G2203A/T) associated with HCC were also analyzed.
Hepatitis B virus mutations, expression quantitative trait loci for PTPN12, and their interactions in hepatocellular carcinoma.
Result: Of those 19 hotspot mutations, C1653T, T1674C/G, A1703G, G1719T, T1727A/G, T1753C, A1762T, G1764A, G1799C, G1899A, G1915A/C, and C1969T were significantly associated with an increased risk of HCC
Discussion: They found that the interactions of rs9277535 AA with the T1674C/G or G1719T mutation in genotype C significantly decreased HCC risk 28.
HBV core promoter mutations and AKT upregulate S-phase kinase-associated protein 2 to promote postoperative hepatocellular carcinoma progression.
Introduction: In addition to TA, other CP mutations, notably C1653T, T1674C/G, C1766T, T1753V and T1768A, have also been reported to be associated with an increased risk of HCC.
Phosphatase and tensin homologue genetic polymorphisms and their interactions with viral mutations on the risk of hepatocellular carcinoma.
Introduction: We and others have reported that HBV mutations C1653T, T1753V, A1762T/G1764A, T1674C/G, and C1766T/T1768A in the enhancer II/basal core promoter (EnhII/BCP) region; G1899A, C2002T, A2159G, A2189C, and G2203A/T in the precore/core region; as well as T53C, PMID: 26447624
2015
Zhonghua gan zang bing za zhi
Abstract: CONCLUSION: Incidence of the T1674C mutation in the X region and of the T1753C mutation and the A1762T/G1764A double mutation in the BCP region was higher for patients with HBV-related HCC; the T1753C mutation and the A1762T/G1764A double mutation may inhibit the formation of HBeAg.
Abstract: The T1674C mutation in the X region, however, occurred more frequently in the HCC group (29.27% vs.6.67%, P<0.05).
Hepatitis B virus genotype, mutations, human leukocyte antigen polymorphisms and their interactions in hepatocellular carcinoma: a multi-centre case-control study.
Method: A risk prediction model to classify the HCC cases and controls was constructed according to the following steps: (1) Prediction factor selection: HBV genotype, the 11 independent HCC-related mutations (C1653T, C1673T, T16
Discussion: They sequenced the HBV EnhII/BCP/PC region successfully from 1,429 (52.2%) of the HBV-infected subjects and found that the interactions of rs9277535 AA with the T1674C/G or G1719T mutation in genotype C significantly decreased HCC risk.
Association of a potential functional pre-miR-218 polymorphism and its interaction with hepatitis B virus mutations with hepatocellular carcinoma risk.
Abstract: CONCLUSION: rs11134527 may be a novel genetic risk factor of Abstract: In multivariate regression analyses, rs11134527 in dominant model was associated with HCC risk (OR = 1.50, 95% CI = 1.05-2.13), whereas its multiplicative interaction with viral mutation T1674C/G was inversely associated with HCC risk (OR = 0.44, 95% CI = 0.21-0.96), adjusting for covariates including HBV mutations in the enhancer II-precore region; its interaction with HBV preS1 start codon mutation was associated with HCC risk (OR = 4.44, 95% CI = 1.27-15.55), adjusting for covariates including HBV mutations in the preS region.
Interaction of signal transducer and activator of transcription 3 polymorphisms with hepatitis B virus mutations in hepatocellular carcinoma.
Abstract: In multivariate regression analyses, multiplicative interaction of rs1053004 with T1674C/G significantly increased HCC risk, whereas rs2293152 and A1726C interaction reduced it, adjusting for covariates including HBV mutations in the enhancer II/basal core promoter/precore region; the interaction of rs4796793 with preS2 start codon mutation significantly increased HCC risk, adjusting for covariates including HBV mutations in the preS region.
Abstract: rs2293152 GG was significantly associated with high viral load (>=1 x 10(4) copies/mL) (AOR, 1.37; 95%, CI 1.01-1.88) and increased frequencies of
Associations of pri-miR-34b/c and pre-miR-196a2 polymorphisms and their multiplicative interactions with hepatitis B virus mutations with hepatocellular carcinoma risk.
Discussion: In the HBV-infected subjects with the data of HBV mutations, however, pri-miR-34b/c rs4938723 CC genotype was significantly associated with increased frequencies of HCC-related HBV mutation T1674C/G (Table 3).
Discussion: miR-34b/c might be involved in immune selection of T1674C/G and this immune selection might be independent of exacerbation during chronic HBV infection.
Discussion: rs4938723 CC genotype and rs11614913 TC genotype might predispose the host to immune selection of T1674C/G, and G1896A, respectively.
HBV mutation literature information.
PMID: 
2022
Frontiers in oncology
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