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Article: Specific mutations in enhancer II/core promoter of hepatitis B virus subgenotypes C1/C2 increase the risk of hepatocellular carcinoma

TitleSpecific mutations in enhancer II/core promoter of hepatitis B virus subgenotypes C1/C2 increase the risk of hepatocellular carcinoma
Authors
KeywordsCore promoter
Enhancer II
Hepatitis B virus
Hepatocellular carcinoma
Precore genome
Subgenotype C
Issue Date2006
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep
Citation
Journal Of Hepatology, 2006, v. 45 n. 5, p. 646-653 How to Cite?
AbstractBackground/Aims: Hepatitis B virus genotype C (HBV/C) has been classified into two geographically distinct subgenotypes; HBV/C1/Cs (Southeast Asia) and HBV/C2/Ce (East Asia). Methods: Viral differences in enhancer II/core promoter and precore regions between the subgenotypes and their association with hepatocellular carcinoma (HCC) were assessed in a matched cross-sectional control study of 118 carriers (from Hong Kong) with HBV/C1/Cs (48.0 years, 81% male, 40% HBeAg+, 44% HCC) and 210 HBV/C2/Ce (172 from Japan, 38 from Hong Kong) (50.2 years, 78% male, 30% HBeAg+, 46% HCC). Results: Univariate analyses showed that mutation V1753 was predictive for HCC among HBeAg-positive-C1/Cs-carriers (P = 0.0055), and T1653 among HBeAg-positive-C2/Ce-carriers (P = 0.018), and T1653 or V1753 or T1762/A1764 among HBeAg-negative-C2/Ce-carriers (P < 0.05). In the multivariate analysis on all HBV/C subjects, independent predictive factors for HCC were subgenotype C2/Ce (odds ratio, 4.21; 95% confidence interval, 1.07-16.23), T1653 (3.64; 1.93-6.86), V1753 (3.07; 1.66-5.65) and T1762/A1764 (2.58; 1.21-5.49) mutations, age (≥50 years), gender (male) and HBeAg (positive). Conclusions: Our data indicate that T1653 and/or V1753 mutations in addition to T1762/A1764 are differently associated with HCC in context of HBeAg status among HBV/C1/Cs and C2/Ce-carriers. HBV/C subgenotypes have specific mutation patterns, which is probably responsible for increased carcinogenesis of HBV/C2/Ce. © 2006 European Association for the Study of the Liver.
Persistent Identifierhttp://hdl.handle.net/10722/77785
ISSN
2015 Impact Factor: 10.59
2015 SCImago Journal Rankings: 4.570
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTanaka, Yen_HK
dc.contributor.authorMukaide, Men_HK
dc.contributor.authorOrito, Een_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorIto, Ken_HK
dc.contributor.authorKurbanov, Fen_HK
dc.contributor.authorSugauchi, Fen_HK
dc.contributor.authorAsahina, Yen_HK
dc.contributor.authorIzumi, Nen_HK
dc.contributor.authorKato, Men_HK
dc.contributor.authorLai, CLen_HK
dc.contributor.authorUeda, Ren_HK
dc.contributor.authorMizokami, Men_HK
dc.date.accessioned2010-09-06T07:35:42Z-
dc.date.available2010-09-06T07:35:42Z-
dc.date.issued2006en_HK
dc.identifier.citationJournal Of Hepatology, 2006, v. 45 n. 5, p. 646-653en_HK
dc.identifier.issn0168-8278en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77785-
dc.description.abstractBackground/Aims: Hepatitis B virus genotype C (HBV/C) has been classified into two geographically distinct subgenotypes; HBV/C1/Cs (Southeast Asia) and HBV/C2/Ce (East Asia). Methods: Viral differences in enhancer II/core promoter and precore regions between the subgenotypes and their association with hepatocellular carcinoma (HCC) were assessed in a matched cross-sectional control study of 118 carriers (from Hong Kong) with HBV/C1/Cs (48.0 years, 81% male, 40% HBeAg+, 44% HCC) and 210 HBV/C2/Ce (172 from Japan, 38 from Hong Kong) (50.2 years, 78% male, 30% HBeAg+, 46% HCC). Results: Univariate analyses showed that mutation V1753 was predictive for HCC among HBeAg-positive-C1/Cs-carriers (P = 0.0055), and T1653 among HBeAg-positive-C2/Ce-carriers (P = 0.018), and T1653 or V1753 or T1762/A1764 among HBeAg-negative-C2/Ce-carriers (P < 0.05). In the multivariate analysis on all HBV/C subjects, independent predictive factors for HCC were subgenotype C2/Ce (odds ratio, 4.21; 95% confidence interval, 1.07-16.23), T1653 (3.64; 1.93-6.86), V1753 (3.07; 1.66-5.65) and T1762/A1764 (2.58; 1.21-5.49) mutations, age (≥50 years), gender (male) and HBeAg (positive). Conclusions: Our data indicate that T1653 and/or V1753 mutations in addition to T1762/A1764 are differently associated with HCC in context of HBeAg status among HBV/C1/Cs and C2/Ce-carriers. HBV/C subgenotypes have specific mutation patterns, which is probably responsible for increased carcinogenesis of HBV/C2/Ce. © 2006 European Association for the Study of the Liver.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhepen_HK
dc.relation.ispartofJournal of Hepatologyen_HK
dc.subjectCore promoteren_HK
dc.subjectEnhancer IIen_HK
dc.subjectHepatitis B virusen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectPrecore genomeen_HK
dc.subjectSubgenotype Cen_HK
dc.subject.meshCarcinoma, Hepatocellular - virology-
dc.subject.meshEnhancer Elements, Genetic-
dc.subject.meshGenome, Viral - genetics-
dc.subject.meshHepatitis B virus - genetics - pathogenicity-
dc.subject.meshHepatitis B, Chronic - genetics - virology-
dc.titleSpecific mutations in enhancer II/core promoter of hepatitis B virus subgenotypes C1/C2 increase the risk of hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0168-8278&volume=45&issue=5&spage=646&epage=653&date=2006&atitle=Specific+mutations+in+enhancer+II/core+promoter+of+hepatitis+B+virus+subgenotypes+C1/C2+increase+the+risk+of+hepatocellular+carcinomaen_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailLai, CL:hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jhep.2006.06.018en_HK
dc.identifier.pmid16935384-
dc.identifier.scopuseid_2-s2.0-33749075767en_HK
dc.identifier.hkuros126116en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33749075767&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue5en_HK
dc.identifier.spage646en_HK
dc.identifier.epage653en_HK
dc.identifier.isiWOS:000241975700003-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridTanaka, Y=35235708000en_HK
dc.identifier.scopusauthoridMukaide, M=6701669224en_HK
dc.identifier.scopusauthoridOrito, E=7006161634en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridIto, K=9242748800en_HK
dc.identifier.scopusauthoridKurbanov, F=7003649588en_HK
dc.identifier.scopusauthoridSugauchi, F=7004837927en_HK
dc.identifier.scopusauthoridAsahina, Y=7003395075en_HK
dc.identifier.scopusauthoridIzumi, N=7102192003en_HK
dc.identifier.scopusauthoridKato, M=7406302992en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.scopusauthoridUeda, R=35376281000en_HK
dc.identifier.scopusauthoridMizokami, M=7103318255en_HK

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