Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Nov 9;10(11):3091.
doi: 10.3390/cells10113091.

Treatment for Viral Hepatitis as Secondary Prevention for Hepatocellular Carcinoma

Saleh A Alqahtani  1   2 , Massimo Colombo  3
Affiliations
Review

Treatment for Viral Hepatitis as Secondary Prevention for Hepatocellular Carcinoma

Saleh A Alqahtani et al. Cells. .

Abstract

Chronic infections with either hepatitis B or C virus (HBV or HCV) are among the most common risk factors for developing hepatocellular carcinoma (HCC). The hepatocarcinogenic potential of these viruses is mediated through a wide range of mechanisms, including the induction of chronic inflammation and oxidative stress and the deregulation of cellular pathways by viral proteins. Over the last decade, effective anti-viral agents have made sustained viral suppression or cure a feasible treatment objective for most chronic HBV/HCV patients. Given the tumorigenic potential of HBV/HCV, it is no surprise that obtaining sustained viral suppression or eradication proves to be effective in preventing HCC. This review summarizes the mechanisms by which HCV and HBV exert their hepatocarcinogenic activity and describes in detail the efficacy of anti-HBV and anti-HCV therapies in terms of HCC prevention. Although these treatments significantly reduce the risk for HCC in patients with chronic viral hepatitis, this risk is not eliminated. Therefore, we evaluate potential strategies to improve these outcomes further and address some of the remaining controversies.

Keywords: HBC; HCC; HCV; hepatocellular carcinoma; prevention.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mechanisms of oncogenesis by HCV and HBV. Percentages indicate the frequency with which the effect is observed in patients with infection-associated HCC. Viral proteins implicated in the oncogenic mechanism are noted.
Figure 2
Figure 2
Mechanisms of HCC prevention and risk persistence following DAA or NA therapy.
See this image and copyright information in PMC

References

    1. WHO International Agency for Research on Cancer GLOBOCAN. [(accessed on 3 December 2020)]. Available online: https://gco.iarc.fr/today/data/factsheets/populations/900-world-fact-she....
    1. Altekruse S.F., McGlynn K.A., Reichman M.E. Hepatocellular Carcinoma Incidence, Mortality, and Survival Trends in the United States from 1975 to 2005. J. Clin. Oncol. 2009;27:1485–1491. doi: 10.1200/JCO.2008.20.7753. - DOI - PMC - PubMed
    1. Valery P.C., Laversanne M., Clark P., Petrick J.L., McGlynn K.A., Bray F. Projections of primary liver cancer to 2030 in 30 countries worldwide. Hepatology. 2017;67:600–611. doi: 10.1002/hep.29498. - DOI - PMC - PubMed
    1. De Martel C., Maucort-Boulch D., Plummer M., Franceschi S. World-wide relative contribution of hepatitis B and C viruses in hepatocellular carcinoma. Hepatology. 2015;62:1190–1200. doi: 10.1002/hep.27969. - DOI - PMC - PubMed
    1. Plummer M., de Martel C., Vignat J., Ferlay J., Bray F., Franceschi S. Global burden of cancers attributable to infections in 2012: A synthetic analysis. Lancet Glob. Health. 2016;4:e609–e616. doi: 10.1016/S2214-109X(16)30143-7. - DOI - PubMed

MeSH terms