The risk of hepatocellular carcinoma among chronic hepatitis B virus‐infected patients outside current treatment criteria

Sinn, Dong Hyun; Kim, Sung Eun; Kim, Seung Up; Kim, Ji Hoon; Choi, Moon Seok

doi:10.1111/jvh.13185

Cited by 42 publications

(39 citation statements)

References 25 publications

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“…Compared with uninfected people, the risk of developing HCC among HBV related CLD patients ranges from 10‐fold to 100‐fold greater 22–24 . The incidence of HCC is increasing with each passing year, causing a rising public health burden worldwide.…”

Section: Discussionmentioning

confidence: 99%

“…Compared with uninfected people, the risk of developing HCC among HBV related CLD patients ranges from 10-fold to 100-fold greater. [22][23][24] The incidence of HCC is increasing with each passing year, causing a rising public health burden worldwide. HBV-related HCC occurs in an environment of inflammation that causes by chronic liver damage, indicating that the development of HCC is immune-mediated.…”

Section: Discussionmentioning

confidence: 99%

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GP73 facilitates hepatitis B virus replication by repressing the NF‐κB signaling pathway

Liu

Zhu

Yang

et al. 2020

Journal of Medical Virology

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Hepatitis B virus (HBV) chronically infects approximately 350 million people worldwide, and 600 000 deaths are caused by HBV‐related hepatic failure. Golgi protein 73 (GP73) is a serum biomarker for liver diseases, including chronic hepatitis B. Here, we determine the effect of HBV infection on GP73 production and characterized the role of GP73 in HBV replication. Initially, we show that GP73 is highly produced in the sera of HBV‐positive patients with chronic liver diseases and in HBV‐stimulated leukocytes. In addition, HBV stimulation promotes GP73 production in peripheral blood mononuclear cells isolated from healthy donors and in macrophages derived from human acute monocytic leukemia cells (THP‐1). Notably, the hepatitis B surface antigen (HBsAg), but not HBV replication, is required for the activation of GP73 expression. Moreover, in HepG2 cells and Huh7 cells, GP73 facilitates HBV replication and represses nuclear factor kappa B p50 expression, which in turn represses HBV replication and GP73 expression. Finally, we demonstrate that GP73 facilitates HBV replication by repressing the innate immune response and the nuclear factor kappa B signaling pathway. Taken together, we revealed a distinct positive feedback mechanism between HBV replication and GP73 production and suggest that GP73 acts as a potential antiviral target for HBV infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

GP73 facilitates hepatitis B virus replication by repressing the NF‐κB signaling pathway

Liu

Zhu

Yang

et al. 2020

Journal of Medical Virology

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“…In another retrospective analysis of 875 patients with chronic HBV infection who received entecavir monotherapy, the probability of HCC in LLV patients during treatment was significantly higher than that in patients with continuous response, and the hazard ratio was 1.98, which is even more pronounced in patients with liver cirrhosis ( 61 ). Therefore, it is important to continue to pay attention to LLV during treatment ( 62 , 63 ).…”

Section: Risk Predictionmentioning

confidence: 99%

Risk Factors and Prevention of Viral Hepatitis-Related Hepatocellular Carcinoma

et al. 2021

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Hepatocellular carcinoma (HCC) is a common cancer in the world, and its incidence is increasing yearly. Hepatitis B virus (HBV) infection and hepatitis C virus (HCV) infection are important causes of HCC. Liver cirrhosis, age, sex, smoking and drinking, and metabolic risk factors will increase the risk of cancer in HBV/HCV patients. And viral load, APRI, FIB-4, and liver stiffness can all predict the risk of HCC in patients with viral infection. In addition, effective prevention strategies are essential in reducing the risk of HCC. The prevention of HCC involves mainly tertiary prevention strategies, while the primary prevention is based on standardized vaccine injections to prevent the occurrence of HBV/HCV. Eliminating the route of transmission and vaccination will lead to a decrease in the incidence of HCC. Secondary prevention involves effective antiviral treatment of HBV/HCV to prevent the disease from progressing to HCC, and tertiary prevention is actively treating HCC to prevent its recurrence.

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“…The burden of liver cancer is increasing [1], and the risk of HBV-related HCC, despite virological and biochemical responses, is still high in the first five years [2], steadily persists over time [3], and remains stable, particularly in patients with cirrhosis [4] or is at least not eliminated [5]. The HCC risk still exists among those patients outside current treatment criteria or even exists in individuals with HBV that has been functionally cleared [6,7]. These above findings suggest that there are some obstinate HCC-driving factors other than viral replication and hepatitis.…”

Section: Introductionmentioning

confidence: 99%

Liver damage favors the eliminations of HBV integration and clonal hepatocytes in chronic hepatitis B

Huang

et al. 2021

Hepatol Int

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Background HBV integration is suspected to be an obstinate risk factor for hepatocellular carcinoma (HCC) in the era of antiviral therapy. Integration events start to occur in the immunotolerance phase, but their fates in the immune clearance phase have not yet been clarified. Here, we report the influences of liver damage on HBV integration and clonal hepatocyte expansion in patients with chronic hepatitis B (CHB). Methods HBV integration breakpoints in liver biopsy samples from 54 CHB patients were detected using a modified next-generation sequencing assay. Results A total of 3729 (69 per sample) integration breakpoints were found in the human genome, including some hotspot genes and KEGG pathways, especially in patients with abnormal transaminases. The number of breakpoint types, an integration risk parameter, was negatively correlated with HBV DNA load and transaminase levels. The average, maximum and total frequencies of given breakpoint types, parameters of clonal hepatocyte expansion, were negatively correlated with HBV DNA load, transaminase levels and liver inflammation activity grade score. The HBV DNA load and inflammation activity grade score were further found to be positively correlated with transaminase levels. Moreover, nucleos(t)ide analog (NUC) treatment that normalized transaminases nonsignificantly reduced the types, but significantly increased the average frequency and negated the enrichments of integration breakpoints. Conclusion Liver damage mainly removed the inventories of viral integration and clonal hepatocytes in CHB. NUC treatment may have reduced HBV integration but clearly increased clonal hepatocyte expansion, which may explain why HCC risk cannot be ruled out by NUC treatment.

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The risk of hepatocellular carcinoma among chronic hepatitis B virus‐infected patients outside current treatment criteria

Cited by 42 publications

References 25 publications

GP73 facilitates hepatitis B virus replication by repressing the NF‐κB signaling pathway

GP73 facilitates hepatitis B virus replication by repressing the NF‐κB signaling pathway

Risk Factors and Prevention of Viral Hepatitis-Related Hepatocellular Carcinoma

Liver damage favors the eliminations of HBV integration and clonal hepatocytes in chronic hepatitis B

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