Result: A1762T/G1764A, T1674G, C1653T, T1674G, and T1753C were all identified as independent risk factors of HCC occurrence in our previous cohort study.
Result: In this cohort of HBV-infected patients, combo mutation
Discussion: We provide evidence supporting the oncogenic function of T1674G+T1753C+A1762T/G1764A (M2) and C1653T+T1674G+A1762T/G1764A (M3) combo mutations.
Genetic diversity in enhancer II region of HBV genotype D and its association with advanced liver diseases.
Abstract: HCC-associated mutations were detected in 33.7% of the sequences, with significantly higher frequency of C1653T, T1753V and A1762T/G1764A in genotype G than C (P < 0.001).
Discussion: A previous meta-analysis showed that Pre-S deletions, C1653T in enhancer II, and T1753V and A1762T/G1764A in BCP are associated with increased risk of HCC compared with HBV without mutations.
Discussion: Genotype C displayed the highest frequency of
The genetic polymorphism down-regulating HLA-DRB1 enhancer activity facilitates HBV persistence, evolution and hepatocarcinogenesis in the Chinese Han population.
Abstract: rs3135395-T, rs477515-T and rs2395178-G were inversely associated with the generation of A1762T/G1764A, T1753V and C1653T, the HCC-risk HBV mutations.
Complete genome analysis of hepatitis B virus in Qinghai-Tibet plateau: the geographical distribution, genetic diversity, and co-existence of HBsAg and anti-HBs antibodies.
Result: Nucleotide mutations, including A1984G, T150AC, A2735C, C2523G, A37G, C2712AT, and C1653T were dramatically different in CD1 and CD2, though these mutations were in the same recombination regions (genotype C or genotype D fragment).
Table: C1653T
Discussion: Other mutations, such as T53C, G1613A, C1653T, T1753C, A2189C, T3098C and PreS deletions were also reported associated with clinical progress.
Discussion: The sa
High possibility of hepatocarcinogenesis in HBV genotype C1 infected Cambodians is indicated by 340 HBV C1 full-genomes analysis from GenBank.
Abstract: Multiple mutations were confirmed in 24 Cambodian C1 isolates, especially double mutation at A1762T/G1764A in 18 isolates (75.0%), and combination mutation at C1653T and/or T1753V and A1762T/G1764A in 14 isolates (58.3%).
Introduction: Mutations at C1653T and/or T1753V and A1762T/G1764A in Enhancer II/basal core promoter were also reported to be associated with HCC in 1999 compared with other liver disease statuses.
Introduction: The c
Large-scale viral genome analysis identifies novel clinical associations between hepatitis B virus and chronically infected patients.
Result: Aside from C1817T and A1838G variants, it is worth mentioning that C1653T, G1896A, and G1899A displayed the next most significant association with viral load in the discovery patient cohort (LRT p = 6 x 10-8, p = 6.7 x 10-8, and p = 2.3 x 10-7, respectively).
Result: Specifically, C1653T alters the binding site of the CAAT enhancer-binding protein of the alpha-box within the HBV enhancer II region, which is known to transcriptionally regulate the pgRNA.
Discussion: C1653T exhibited only marginal signal with viral load.
Discussion: Previous studies described additional variants in the core promoter including
Locus 5p13.1 may be associated with the selection of cancer-related HBV core promoter mutations.
PMID: 31341412
2019
International journal of medical sciences
Introduction: The precore mutation (G1896A), mutations in enhancer II (C1653T) and the BCP (T1753V and the double mutations, A1762T, G1764A), and deletions in the pre-S region have been reported to be associated with the development of HCC.
Next generation sequencing identifies baseline viral mutants associated with treatment response to pegylated interferon in HBeAg-positive chronic hepatitis B.
Abstract: No significant difference between groups was found regarding C1653T and G1896A mutants.
The mutation of hepatitis B virus and the prognosis of hepatocellular carcinoma after surgery: a pilot study.
PMID: 29628773
2018
Cancer management and research
Introduction: The X gene mutations (two of the most common being C1653T and T1753V) and Pre S2 gene deletions have been associated with increased incidence of HCC.
HBV mutation literature information.
PMID: 
2022
Frontiers in oncology
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