Hepatitis B virus–induced hepatocarcinogenesis: A virological and oncological perspective

Arslan, Ferhat; Franci, Gianluigi; Nastri, Bianca Maria; Pagliano, Pasquale

doi:10.1111/jvh.13551

Cited by 9 publications

(7 citation statements)

References 58 publications

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“…[25] Since the majority (up to 90%) of the HBsAg is transcribed from integrated HBV DNA (iDNA) in patients with HBeAg-negative CHB [26][27][28] and iDNA is strongly correlated with HBsAg level, [29] perhaps the greater qHBsAg decline and lower end of follow-up qHBsAg have reduced transcriptional activity of iDNA, an important cause of HBV carcinogenesis by means of its production of viral oncogenic protein, for example, HBx. [30][31][32] In contrast, continued Nuc therapy can interrupt new HBV DNA integration but not inhibit transcription from iDNA. [28] Hence, finite therapy had lower HCC incidence than those continued therapy.…”

Section: Discussionmentioning

confidence: 99%

“…Likewise, it was demonstrated that lower HBsAg level correlated with lower long-term HCC recurrence and longer survival in a study of 522 patients with HBV-HCC who had received curative resection and Nuc treatment 25 . Since the majority (up to 90%) of the HBsAg is transcribed from integrated HBV DNA (iDNA) in patients with HBeAg-negative CHB 26–28 and iDNA is strongly correlated with HBsAg level, 29 perhaps the greater qHBsAg decline and lower end of follow-up qHBsAg have reduced transcriptional activity of iDNA, an important cause of HBV carcinogenesis by means of its production of viral oncogenic protein, for example, HBx 30–32 . In contrast, continued Nuc therapy can interrupt new HBV DNA integration but not inhibit transcription from iDNA 28 .…”

Section: Discussionmentioning

confidence: 99%

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Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis

Jeng,

Chien,

Chen

et al. 2023

Hepatology

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Background & Aims: Long-term nucleos(t)ide analogue (Nuc) treatment can reduce hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV)-related cirrhosis (HBV-LC). Earlier small cohort studies showed a comparable 5-year incidence of HCC in hepatitis B e antigen (HBeAg)-negative HBV-LC patients who stopped and those continued Nuc therapy. This study aimed to validate these findings using a large cohort with 10-year follow-up. Approach & Results: From two centers, 494 HBeAg-negative HBV-LC patients who stopped (finite group) and 593 who continued (continuous group) Nuc therapy were recruited. HCC, hepatitis B surface antigen (HBsAg) loss, liver-related mortality/transplantation and overall survival rates were compared between two groups with 1:1 propensity score matching (PSM) of gender, prior treatment history, types of Nuc, age, transaminases, platelet count, and HBsAg levels at end-of-therapy (EOT) in finite group or 3-year-on-therapy in continuous groups. During a median follow-up of 6.2 (3.4-8.9) years, the annual and 10-year HCC incidence were lower in finite group (1.6 vs. 3.3%/year and 10-year 15.7 vs. 26.8%, respectively; Log-rank test, p<0.0001). The finite group showed greater HBsAg decline/year (-0.116 vs. -0.095 log10 IU/mL, p=0.0026) and 7-8 times higher 10-year incidence of HBsAg loss (22.7 vs. 3%, p<0.0001). Multivariate Cox regression showed finite therapy an independent protective factor for HCC [adjusted hazard ratio(aHR): 0.593], liver-related mortality/transplantation (aHR: 0.312) and overall mortality (aHR: 0.382). Conclusions: Finite Nuc therapy in HBeAg-negative HBV-LC may reduce HCC incidence, increase HBsAg loss and improve survival. Greater HBsAg decline/loss may reflect enhanced immunity and contribute to the reduction of hepatic carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis

Jeng,

Chien,

Chen

et al. 2023

Hepatology

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“…Recently, it has also been suggested that alterations of hemostasis, particularly of platelets, could have a role in hepatocarcinogenesis [ 35 , 36 ]. Additional mechanisms that promote the induction of HCC in patients with HBV, HCV, and HBV-HDV infection are discussed below ( Table 1 ) [ 37 , 38 , 39 , 40 , 41 , 42 , 43 ].…”

Section: Viral-related Hepatic Carcinogenesismentioning

confidence: 99%

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Russo

Zanetto

Pinto

et al. 2022

IJMS

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Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related death. Although the burden of alcohol- and NASH-related HCC is growing, chronic viral hepatitis (HBV and HCV) remains a major cause of HCC development worldwide. The pathophysiology of viral-related HCC includes liver inflammation, oxidative stress, and deregulation of cell signaling pathways. HBV is particularly oncogenic because, contrary to HCV, integrates in the cell DNA and persists despite virological suppression by nucleotide analogues. Surveillance by six-month ultrasound is recommended in patients with cirrhosis and in “high-risk” patients with chronic HBV infection. Antiviral therapy reduces the risks of development and recurrence of HCC; however, patients with advanced chronic liver disease remain at risk of HCC despite virological suppression/cure and should therefore continue surveillance. Multiple scores have been developed in patients with chronic hepatitis B to predict the risk of HCC development and may be used to stratify individual patient’s risk. In patients with HCV-related liver disease who achieve sustained virological response by direct acting antivirals, there is a strong need for markers/scores to predict long-term risk of HCC. In this review, we discuss the most recent advances regarding viral-related HCC.

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“…HBV has been demonstrated to as a common etiological factor for hepatocarcinogenesis worldwide ( Amaddeo et al, 2015 ; Arslan et al, 2021 ). Emerging studies have been indicated that the TRIM family not only contributed to the progression of HCC but also participated in the modulation of HBV infection ( Fan et al, 2019 ; Liu et al, 2020 ; Mu et al, 2020 ), while to date, the relationship of TRIM with HBV-associated hepatocarcinogenesis is not well investigated.…”

Section: Discussionmentioning

confidence: 99%

“…In the eastern Pacific region and Africa, the chronic infection of hepatitis B virus (HBV) is still a predominant risk factor for the initiation and development of hepatoma carcinoma (HCC) ( Geng et al, 2015 ; Jia et al, 2020 ; Arslan et al, 2021 ; Jiang Y. et al, 2021 ). The occurrence and progress of HCC have a close association with various cellular factors regulated by HBV.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Analysis of TRIM Family Genes in Hepatitis Virus B-Related Hepatoma Carcinoma

Li²,

Li³

et al. 2022

Front. Genet.

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Background: As significant components of E3 ligases, the tripartite motif (TRIM) proteins participate in various biological processes and facilitate the development of several diseases. Nevertheless, the correlations of TIRMs with hepatitis B virus (HBV)-positive hepatoma carcinoma (HCC) are not well elaborated.Methods: The expression profile of TRIM genes in HBV-associated HCC and related clinical information were extracted from the Cancer Genome Atla (TCGA) database and the International Cancer Genome Consortium (ICGC) database. Dependent on the ConsensusPathDB and STRING databases, the gene ontology, Reactome pathways, and protein-protein interaction were assessed. Relied on TIMER 2.0 database, the relationship of the TRIMs with immune infiltration was investigated. Using multivariate analysis and Kaplan Meier analysis, the association between TRIM genes and the prognostic value was examined.Results: A total of 17 TRIM genes, including TRIM16, TRIM17, and TRIM31 with fold change no less than 1.5, were discovered to upregulate in HBV-associated HCC in both TCGA and ICGC cohorts. Relied on gene enrichment analysis, the identified TRIMs were observed to not only be related to the interferon and cytokine signaling but also linked to the adaptive immune system. Particularly, the co-expression patterns of identified TRIMs with other E3 ligase genes and many innate immune genes that are associated with Toll-like receptor signaling, apoptosis, and SUMOylation. Besides, some of identified TRIM expressions were also linked to the infiltration levels of T cells and B cells. Additionally, several TRIM genes were associated with various clinical factors and relevant to the poor survival of HBV-associated HCC.Conclusion: Our findings could deepen our understanding of TRIMs and their correlations with HBV-associated HCC. Furthermore, some of these TRIMs may be utilized as new prognostic markers of HBV-related HCC prognosis, or act as potential molecular targets for the disease.

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Hepatitis B virus–induced hepatocarcinogenesis: A virological and oncological perspective

Cited by 9 publications

References 58 publications

Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis

Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Comprehensive Analysis of TRIM Family Genes in Hepatitis Virus B-Related Hepatoma Carcinoma

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