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      Epidemiology of Hepatitis B Virus (HBV) and Hepatitis C Virus (HCV) Related Hepatocellular Carcinoma

      review-article
      *
      The Open Virology Journal
      Bentham Open
      Hepatocellular carcinoma, HBV, HCV, HCC, Epidemiology, Risk factors

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          Abstract

          Introduction:

          Hepatocellular carcinoma (HCC) is one of the most prevalent primary malignant tumors and accounts for about 90% of all primary liver cancers. Its distribution varies greatly according to geographic location and it is more common in middle and low- income countries than in developed ones especially in Eastern Asia and Sub Saharan Africa (70% of all new HCCs worldwide), with incidence rates of over 20 per 100,000 individuals.

          Explanation:

          The most important risk factors for HCC are Hepatitis B Virus (HBV) infection, Hepatitis C Virus (HCV) infection, excessive consumption of alcohol and exposition to aflatoxin B1. Its geographic variability and heterogeneity have been widely associated with the different distribution of HBV and HCV infections worldwide.

          Chronic HBV infection is one of the leading risk factors for HCC globally accounting for at least 50% cases of primary liver tumors worldwide. Generally, while HBV is the main causative agent in the high incidence HCC areas, HCV is the major etiological factor in low incidence HCC areas, like Western Europe and North America.

          Conclusion:

          HBV-induced HCC is a complex, stepwise process that includes integration of HBV DNA into host DNA at multiple or single sites. On the contrary, the cancerogenesis mechanism of HCV is not completely known and it still remains controversial as to whether HCV itself plays a direct role in the development of tumorigenic progression.

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          Most cited references45

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          Hepatocellular carcinoma: epidemiology, risk factors and pathogenesis.

          Hepatocellular carcinoma (HCC) is the commonest primary malignant cancer of the liver in the world. Given that the burden of chronic liver disease is expected to rise owing to increasing rates of alcoholism, hepatitis B and C prevalence and obesity-related fatty liver disease, it is expected that the incidence of HCC will also increase in the foreseeable future. This article summarizes the international epidemiology, the risk factors and the pathogenesis of HCC, including the roles of viral hepatitis, toxins, such as alcohol and aflatoxin, and insulin resistance.
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            Hepatitis B virus x protein in the pathogenesis of hepatitis B virus-induced hepatocellular carcinoma.

            James Kew (2010)
            Currently available evidence supports a role for the hepatitis B virus (HBV) x gene and protein in the pathogenesis of HBV-induced hepatocellular carcinoma (HCC). HBx gene is often included, and remains functionally active, in the HBV DNA that is frequently integrated into cellular DNA during hepatocellular carcinogenesis. HBx protein promotes cell cycle progression, inactivates negative growth regulators, and binds to and inhibits the expression of p53 tumour suppressor gene and other tumour suppressor genes and senescence-related factors. However, the molecular mechanisms responsible for HBx protein-induced HCC remain uncertain. Only some of the more fully documented or more recently recognised mechanisms are reviewed. During recent years evidence has accumulated that HBx protein modulates transcription of methyl transferases, causing regional hypermethylation of DNA that results in silencing of tumour suppressor genes, or global hypomethylation that results in chromosomal instability, thereby playing a role in hepatocarcinogenesis. HBx protein has both anti-apoptotic and pro-apoptotic actions, apparently contradictory effects that have yet to be explained. Particularly important among the anti-apoptotic properties is inhibition of p53. Recent experimental observations suggest that HBx protein may increase the expression of TERT and telomerase activity, prolonging the life-span of hepatocytes and contributing to malignant transformation. The protein also interferes with nucleotide excision repair through both p53-dependent and p53- independent mechanisms. Carboxy-terminal truncated HBx protein loses its inhibitory effects on cell proliferation and pro-apoptotic properties, and it may enhance the protein's ability to transform oncogenes. Dysregulation of IGF-II enhances proliferation and anti-apoptotic effects of oncogenes, resulting in uncontrolled cell growth. © 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.
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              Hepatocellular carcinoma: epidemiology, risk factors, and screening.

              In this article, the epidemiology of hepatocellular carcinoma (HCC), risk factors for the development of HCC, and how these factors affect the decision about whether an individual should or should be entered into a screening program are considered. The factors determining the risk for HCC include age, male gender, and the nature of the underlying liver disease. In particular, cirrhosis is associated with a significant risk for HCC. However, in hepatitis B HCC also occurs in noncirrhotic liver. Decision analysis can be used to identify patients at greatest risk for HCC and who might be candidates for screening. Screening itself should be developed in a programmatic manner to ensure that appropriate target populations are identified, that appropriate screening tests are chosen, and that appropriate recall and enhanced follow-up are instituted for patients who have positive screening test results. Screening should be by ultrasonography at 4- to 12-month intervals. Patients with abnormal screening tests require additional investigation using computed tomography scanning, magnetic resonance imaging, or liver biopsy. Negative results do not exclude the possibility of cancer and further follow-up is necessary.
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                Author and article information

                Journal
                Open Virol J
                Open Virol J
                TOVJ
                The Open Virology Journal
                Bentham Open
                1874-3579
                28 February 2018
                2018
                : 12
                : 26-32
                Affiliations
                [1]Department of Pathology, Virology and Molecular Biology Unit, Istituto Nazionale Tumori- IRCCS Fondazione G. Pascale, Naples, Italy
                Author notes
                [* ]Address correspondence to this author at the Department of Pathology, Virology and Molecular Biology Unit, Arnolfo Petruzziello, Istituto Nazionale Tumori- IRCCS Fondazione G. Pascale, Naples, Italy; Tel:+390815903373; E-mail: a.petruzziello@ 123456istitutotumori.na.it
                Article
                TOVJ-12-26
                10.2174/1874357901812010026
                5842386
                29541276
                ee72aec7-2d95-4a43-89bf-bab124cb80f2
                © 2018 Arnolfo Petruzziello.

                This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 28 August 2017
                : 26 September 2017
                : 02 January 2018
                Categories
                Virology
                Suppl-1, M3

                Microbiology & Virology
                hepatocellular carcinoma,hbv,hcv,hcc,epidemiology,risk factors
                Microbiology & Virology
                hepatocellular carcinoma, hbv, hcv, hcc, epidemiology, risk factors

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