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Article: Role of hepatitis B virus genotypes Ba and C, core promoter and precore mutations on hepatocellular carcinoma: A case control study

TitleRole of hepatitis B virus genotypes Ba and C, core promoter and precore mutations on hepatocellular carcinoma: A case control study
Authors
Issue Date2004
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2004, v. 25 n. 9, p. 1593-1598 How to Cite?
AbstractThe role of hepatitis B virus (HBV) genotypes, core promoter (CP) and precore mutants on hepatocellular carcinoma (HCC) is still controversial. We aimed to determine their role on the development and clinical features of HCC. HBV genotypes and CP/precore mutations were determined in 90 HCC patients and 180 matched control patients. In the 90 HCC patients, 22 (24.4%) and 68 (75.6%) had subtype Ba and genotype C, respectively. The prevalence of genotype C and CP mutations was significantly higher in HCC patients compared with controls (75.6 versus 57.8%, P = 0.004; 90.9 versus 74.8%, respectively, P = 0.007). Among carriers of genotype C, 91.8 % of the HCC patients and 88.8% of controls had CP mutations. Among carriers of subtype Ba, HCC patients had a higher prevalence of CP mutations compared with controls (88.2 versus 54.5%, respectively, P = 0.02). By logistic regression analysis, the only factor associated with HCC was a mutation of the CP region (P = 0.032). There were no differences in the clinical features on presentation, the chance of receiving treatment and the cumulative survival rate for chemoembolization-treated patients between patients with subtype Ba and genotype C. There was too small a number of CP wild-type to do a similar comparison with CP mutants. In conclusion, there was a significantly higher prevalence of both genotype C and CP mutations in patients with HCC. The association between HBV genotype C and HCC was probably not genuine but was due to the high percentage of CP mutations in patients with genotype C. © Oxford University Press 2004; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/76825
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorTanaka, Yen_HK
dc.contributor.authorMizokami, Men_HK
dc.contributor.authorYuen, JCHen_HK
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorYuan, HJen_HK
dc.contributor.authorSum, SMen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2010-09-06T07:25:19Z-
dc.date.available2010-09-06T07:25:19Z-
dc.date.issued2004en_HK
dc.identifier.citationCarcinogenesis, 2004, v. 25 n. 9, p. 1593-1598en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76825-
dc.description.abstractThe role of hepatitis B virus (HBV) genotypes, core promoter (CP) and precore mutants on hepatocellular carcinoma (HCC) is still controversial. We aimed to determine their role on the development and clinical features of HCC. HBV genotypes and CP/precore mutations were determined in 90 HCC patients and 180 matched control patients. In the 90 HCC patients, 22 (24.4%) and 68 (75.6%) had subtype Ba and genotype C, respectively. The prevalence of genotype C and CP mutations was significantly higher in HCC patients compared with controls (75.6 versus 57.8%, P = 0.004; 90.9 versus 74.8%, respectively, P = 0.007). Among carriers of genotype C, 91.8 % of the HCC patients and 88.8% of controls had CP mutations. Among carriers of subtype Ba, HCC patients had a higher prevalence of CP mutations compared with controls (88.2 versus 54.5%, respectively, P = 0.02). By logistic regression analysis, the only factor associated with HCC was a mutation of the CP region (P = 0.032). There were no differences in the clinical features on presentation, the chance of receiving treatment and the cumulative survival rate for chemoembolization-treated patients between patients with subtype Ba and genotype C. There was too small a number of CP wild-type to do a similar comparison with CP mutants. In conclusion, there was a significantly higher prevalence of both genotype C and CP mutations in patients with HCC. The association between HBV genotype C and HCC was probably not genuine but was due to the high percentage of CP mutations in patients with genotype C. © Oxford University Press 2004; all rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshCarcinoma, Hepatocellular - virologyen_HK
dc.subject.meshCarrier Stateen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHepatitis B - complicationsen_HK
dc.subject.meshHepatitis B virus - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLiver Neoplasms - virologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutation - geneticsen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshRisk Factorsen_HK
dc.titleRole of hepatitis B virus genotypes Ba and C, core promoter and precore mutations on hepatocellular carcinoma: A case control studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=25&issue=9&spage=1593&epage=1598&date=2004&atitle=Role+of+hepatitis+B+virus+genotypes+Ba+and+C,+core+promoter+and+precore+mutations+on+hepatocellular+carcinoma:+a+case+control+studyen_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailWong, DKH:danywong@hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.emailLai, CL:hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgh172en_HK
dc.identifier.pmid15090469-
dc.identifier.scopuseid_2-s2.0-4544278536en_HK
dc.identifier.hkuros107559en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4544278536&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1593en_HK
dc.identifier.epage1598en_HK
dc.identifier.isiWOS:000223588800006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridTanaka, Y=7405315865en_HK
dc.identifier.scopusauthoridMizokami, M=7103318255en_HK
dc.identifier.scopusauthoridYuen, JCH=7102620480en_HK
dc.identifier.scopusauthoridWong, DKH=7401535819en_HK
dc.identifier.scopusauthoridYuan, HJ=7402446707en_HK
dc.identifier.scopusauthoridSum, SM=6603889132en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK

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