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Article: Hepatitis B and C virus-related carcinogenesis

TitleHepatitis B and C virus-related carcinogenesis
Authors
Issue Date2009
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLM
Citation
Clinical Microbiology And Infection, 2009, v. 15 n. 11, p. 964-970 How to Cite?
AbstractChronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are the most important causes of hepatocellular carcinoma (HCC), accounting for the majority of the cases worldwide. The geographical distribution of HCC therefore coincides with the distribution of HBV and HCV infections in those areas. Similar to nonviral liver diseases, HBV and HCV infection can cause chronic injury to the liver, with subsequent progression to severe fibrosis and cirrhosis. The presence of cirrhosis is a major risk factor for the development of HCC. However, HCC can occur in the absence of cirrhosis, suggesting that both HBV and HCV may be directly involved in hepatocarcinogenesis. Several HBV factors have been implicated in hepatocarcinogenesis, including the HBx gene, the pre-S2/S gene and the HBV spliced protein. Furthermore, HBV can be integrated into the host genome, leading to changes in genomic function or chromosomal instability. By contrast to HBV, HCV cannot integrate into the host genome. Various HCV proteins, including the core, envelope and nonstructural proteins, have been shown to have oncogenic properties. For HBV infection, antiviral therapy and vaccination have been shown to decrease the risk of HCC. Antiviral therapy for HCV can also reduce the risk of HCC. © 2009 The Authors. Journal Compilation © 2009 European Society of Clinical Microbiology and Infectious Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/163283
ISSN
2015 Impact Factor: 4.575
2015 SCImago Journal Rankings: 2.530
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFung, Jen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorYuen, MFen_US
dc.date.accessioned2012-09-05T05:29:36Z-
dc.date.available2012-09-05T05:29:36Z-
dc.date.issued2009en_US
dc.identifier.citationClinical Microbiology And Infection, 2009, v. 15 n. 11, p. 964-970en_US
dc.identifier.issn1198-743Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/163283-
dc.description.abstractChronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are the most important causes of hepatocellular carcinoma (HCC), accounting for the majority of the cases worldwide. The geographical distribution of HCC therefore coincides with the distribution of HBV and HCV infections in those areas. Similar to nonviral liver diseases, HBV and HCV infection can cause chronic injury to the liver, with subsequent progression to severe fibrosis and cirrhosis. The presence of cirrhosis is a major risk factor for the development of HCC. However, HCC can occur in the absence of cirrhosis, suggesting that both HBV and HCV may be directly involved in hepatocarcinogenesis. Several HBV factors have been implicated in hepatocarcinogenesis, including the HBx gene, the pre-S2/S gene and the HBV spliced protein. Furthermore, HBV can be integrated into the host genome, leading to changes in genomic function or chromosomal instability. By contrast to HBV, HCV cannot integrate into the host genome. Various HCV proteins, including the core, envelope and nonstructural proteins, have been shown to have oncogenic properties. For HBV infection, antiviral therapy and vaccination have been shown to decrease the risk of HCC. Antiviral therapy for HCV can also reduce the risk of HCC. © 2009 The Authors. Journal Compilation © 2009 European Society of Clinical Microbiology and Infectious Diseases.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLMen_US
dc.relation.ispartofClinical Microbiology and Infectionen_US
dc.subject.meshCarcinoma, Hepatocellular - Epidemiology - Virologyen_US
dc.subject.meshHepacivirus - Pathogenicityen_US
dc.subject.meshHepatitis B Virus - Pathogenicityen_US
dc.subject.meshHepatitis B, Chronic - Complications - Epidemiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshViral Proteins - Physiologyen_US
dc.subject.meshVirulence Factors - Physiologyen_US
dc.titleHepatitis B and C virus-related carcinogenesisen_US
dc.typeArticleen_US
dc.identifier.emailFung, J:jfung@sicklehut.comen_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.authorityFung, J=rp00518en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1469-0691.2009.03035.xen_US
dc.identifier.pmid19874379-
dc.identifier.scopuseid_2-s2.0-70449134824en_US
dc.identifier.hkuros174500-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70449134824&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume15en_US
dc.identifier.issue11en_US
dc.identifier.spage964en_US
dc.identifier.epage970en_US
dc.identifier.isiWOS:000271055600002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridFung, J=23091109300en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.citeulike6032931-

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