Downregulation of GSK3β and Upregulation of URG7 in Hepatitis B-Related Hepatocellular Carcinoma

Javanmard, Davod; Niya, Mohammad Hadi Karbalaie; Khalafkhany, Davod; Najafi, Mohammad; Ziaee, Masood; Babaei, Mohammad Reza; Kiani, Seyed Jalal; Esghaei, Maryam; Jazayeri, Seyed Mohammad; Panahi, Mahshid; Tameshkel, Fahimeh Safarnezhad; Mehrabi, Maryam; Monavari, Seyed Hamidreza; Bokharaei‐Salim, Farah

doi:10.5812/hepatmon.100899

Cited by 2 publications

(1 citation statement)

References 51 publications

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“…The HBV DNA load was determined using a real-time PCR assay, as described previously (20). Detection of HBV cccDNA in liver tissue specimens was conducted by a probe-based real-time PCR method, using a Rotor-Gene device (QIAGEN, Germany), as previously explained (21).…”

Section: Detection Of Viral Load and Cccdnamentioning

confidence: 99%

Molecular Investigation of Occult Hepatitis B Virus Infection Among Patients with Liver Cancers

Javanmard,

Marjani,

Karbalaie Niya

et al. 2023

Int J Cancer Manag

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Background: Hepatitis B virus (HBV) is still the leading cause of hepatocellular carcinoma (HCC). HBV could persist in the low replicate state that is defines as occult hepatitis B virus infection (OBI). Recently, OBI has been defined important in the development and/or exacerbation of HCC and other liver diseases. Objectives: This study tried to determine the frequency of OBI among liver tumor samples. Methods: This cross-sectional study was performed among patients with HCC and intrahepatic cholangiocarcinoma (iCCA) in hospitals affiliated with Iran University of Medical Sciences. Liver tumor samples (Fresh frozen and formalin fixed paraffin embedded) were processed for isolation of DNA and then subjected to molecular assays, including PCR examinations of HBV genes (S, X, and C), determination of viral loads, detection of HBV-cccDNA, phylogenetic analysis, and assessment of mutations in HBsAg and RT regions. Results: In total, there were 93 participants, including HCC (n = 60), iCCA (n = 33); among which, 15% were detected positive for OBI. The OBI among HCC and iCCA were 18.3% and 9.1%, respectively. The mean intrahepatic viral load was 1.3 × 105 ± 1.4 × 102 copies/µl, and 5 had detectable cccDNA. The OBI subjects belonged to the HBV genotype D and subgenotype D1. In the HBsAg protein, T45N (33.3%) and P105A (25%) were the most prevalent mutations. N53K (33.3%), Y54H (25%), L80I (33.3%), and A113G (25%) were missense mutations that were observed in the RT domain. Conclusions: HBV-DNA was detected among liver tumor samples with negative HBsAg status. The results of viral load and cccDNA tests are important in identification and prognosis of liver diseases. It’s needed more precise molecular and cohort studies to clarify the functions of OBI in liver diseases.

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Section: Detection Of Viral Load and Cccdnamentioning

confidence: 99%

Molecular Investigation of Occult Hepatitis B Virus Infection Among Patients with Liver Cancers

Javanmard,

Marjani,

Karbalaie Niya

et al. 2023

Int J Cancer Manag

Self Cite

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Whole genome analysis of hepatitis B virus before and during long-term therapy in chronic infected patients: Molecular characterization, impact on treatment and liver disease progression

et al. 2022

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Hepatitis B virus (HBV) infection remains a serious public health concern worldwide despite the availability of an efficient vaccine and the major improvements in antiviral treatments. The aim of the present study is to analyze the mutational profile of the HBV whole genome in ETV non-responder chronic HBV patients, in order to investigate antiviral drug resistance, immune escape, and liver disease progression to Liver Cirrhosis (LC) or Hepatocellular Carcinoma (HCC). Blood samples were collected from five chronic hepatitis B patients. For each patient, two plasma samples were collected, before and during the treatment. Whole genome sequencing was performed using Sanger technology. Phylogenetic analysis comparing the studied sequences with reference ones was used for genotyping. The mutational profile was analyzed by comparison with the reference sequence M32138. Genotyping showed that the studied strains belong to subgenotypes D1, D7, and D8. The mutational analysis showed high genetic variability. In the RT region of the polymerase gene, 28 amino acid (aa) mutations were detected. The most significant mutations were the pattern rtL180M + rtS202G + rtM204V, which confer treatment resistance. In the S gene, 35 mutations were detected namely sP120T, sT126S, sG130R, sY134F, sS193L, sI195M, and sL216stop were previously described to lead to vaccine, immunotherapy, and/or diagnosis escape. In the C gene, 34 mutations were found. In particular, cG1764A, cC1766G/T, cT1768A, and cC1773T in the BCP; cG1896A and cG1899A in the precore region and cT12S, cE64D, cA80T, and cP130Q in the core region were associated with disease progression to LC and/or HCC. Other mutations were associated with viral replication increase including cT1753V, cG1764A/T, cC1766G/T, cT1768A, and cC1788G in the BCP as well as cG1896A and cG1899A in the precore region. In the X gene, 30 aa substitutions were detected, of which substitutions xT36D, xP46S, xA47T, xI88F, xA102V, xI127T, xK130M, xV131I, and xF132Y were previously described to lead to LC and/or HCC disease progression. In conclusion, our results show high genetic variability in the long-term treatment of chronic HBV patients causing several effects. This could contribute to guiding national efforts to optimize relevant HBV treatment management in order to achieve the global hepatitis elimination goal by 2030.

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Downregulation of GSK3β and Upregulation of URG7 in Hepatitis B-Related Hepatocellular Carcinoma

Cited by 2 publications

References 51 publications

Molecular Investigation of Occult Hepatitis B Virus Infection Among Patients with Liver Cancers

Molecular Investigation of Occult Hepatitis B Virus Infection Among Patients with Liver Cancers

Whole genome analysis of hepatitis B virus before and during long-term therapy in chronic infected patients: Molecular characterization, impact on treatment and liver disease progression

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