Molecular characterisation of hepatitis B virus in the resident Chinese population in Panama City.
PMID: 23903967
2013
Memorias do Instituto Oswaldo Cruz
Result: The analysis of mutations in the Enh II, PC and BCP regions of the 10 samples revealed the following results: the mutation G1613A was identified in two samples (20%), two samples (20%) had the mutation pair A1762T/G1764A and one sample carried both G1896A and the A1762T/G1764A double mutation.
Discussion: Mutation analysis in the Enh II region found the G1613A mutation in two subjects; although both samples were HBeAg-positive, in vitro studies have linked this mutation with HBeAg suppression in PMID: 22136288
2012
Cancer science
Abstract: Eight high-frequency mutations (G1613A, C1653T, T1753V, A1762T, G1764A, A1846T, G1896A and G1899A) were significantly associated with HCC.
Precore mutation of hepatitis B virus may contribute to hepatocellular carcinoma risk: evidence from an updated meta-analysis.
Introduction: Those mutations include G1613A, C1653T in the EnhII region; T1753V, the double mutation A1762T/G1764A at the BCP region, G1896A and G1899A in the precore region.
The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity.
Abstract: In summary, our results suggest the functional consequences of the hotspot G1613A mutation found in HBV.
Abstract: Intriguingly, RFX1 binds to the G1613A mutant with higher affinity than the wild-type sequence, indicating that the mutation possesses the trans-activating effect to the core promoter via NRE.
Abstract: Previously, we demonstrated that the G1613A mutation in the HBV negative regulatory element (NRE) is a hotspot mutation in HCC patients.
Abstract: We showed that the G1613A mutation significantly suppresses the secretion of e antigen (HBeAg) and enhances the synthesis of viral DNA, which is in consistence to our clinical result that the
The G1613A mutation in the HBV genome affects HBeAg expression and viral replication through altered core promoter activity.
Abstract: A comparison of the nucleotide sequences of the HBV genome between HCC group 1 and non-HCC group 1 revealed that the prevalence of G1613A and C1653T mutations in the core promoter region was significantly higher in the HCC group.
Abstract: A single G1613A mutation was associated with future emergence of HCC.
Abstract: CONCLUSIONS: G1613A and C1653T double mutations were frequently found in patients with HCC.
Abstract: Future emergence of PMID: 20699378
2010
Cancer epidemiology, biomarkers & prevention
Abstract: RESULTS: The pre-S deletion and 12 point mutations, namely, the pre-S2 start codon mutation, T53C in the pre-S2 gene, T766A in the S gene, G1613A, C1653T, A1762T, G1764A in the X gene, and G1899A, C2002T, A2159G, A2189C, and G2203W (A or T) in the pre-C/C gene, showed close associations with
A case-control study on sequence variations in the enhancer II/core promoter/precore and X genes of hepatitis B virus in patients with hepatocellular carcinoma.
Abstract: No significant difference between groups was found with respect to G1613A, C1653T, C1766T/T1768A, A1846T/C, T1858C, and G1896A mutations.
Associations between hepatitis B virus mutations and the risk of hepatocellular carcinoma: a meta-analysis.
PMID: 19574418
2009
Journal of the National Cancer Institute
Table: G1613A
Discussion: Other mutations that have been shown to be statistically significantly associated with the risk of HCC, such as those at T31C, T53C, G1613A, A1703G, G1719T, C1726A, and G1730C, were not included because few patients had these mutations.
Genotype-specific genomic markers associated with primary hepatomas, based on complete genomic sequencing of hepatitis B virus.
Abstract: HCC-related mutations T31C, T53C, and A1499G were associated with HBV subgenotype Ce, and mutations G1613A, G1899A, T2170C/G, and T2441C were associated with HBV subgenotype Cs.
Hepatitis B virus genomic sequence in the circulation of hepatocellular carcinoma patients: comparative analysis of 40 full-length isolates.
Abstract: G-to-A at nt 1613 and C-to-T at nt 1653 within enhancer II and T-to-C/A at nt 1753 within core promoter were also evident: 38%, 53%, and 40%, respectively.
HBV mutation literature information.
PMID: 
2013
Memorias do Instituto Oswaldo Cruz
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