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Conference Paper: Role of HBV genotypes, core promoter/precore mutations and HBV DNA levels on hepatocarcinogenesis

TitleRole of HBV genotypes, core promoter/precore mutations and HBV DNA levels on hepatocarcinogenesis
Authors
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep
Citation
The 42nd Annual Meeting of the European Association for the Study of the Liver, Barcelona, Spain, 11-15 April 2007. In Journal of Hepatology, 2007, v. 46 n. S1, p. S184-S185 Abstract no. 485 How to Cite?
AbstractAims: To examine whether genotypesicore promoter (CP)/precore variants are independent risk factors for HCC and to define the low risk HBVDNA level in HCC. Patients and Methods: 248 HCC patients and 248 control patients matched for gender, age and HBeAg status were recruited. Results: Compared to controls, HCC patients had a higher prevalence of genotype C [57.4% vs 7 I .7% respectively, p = 0.00 I, O.R. I .9 (95% CT I .3-2.8)] and CP mutations [66.8% vs. 88.1% respectively, p i 0.001, O.R. 3.7 (95% CT 2.1-6.3)]. Prevalence of precore mutations was comparable between 2 groups. Multivariate analysis revealed CP mutations as the only independent risk factor for HCC (p i 0.001). CP mutations was associated with a specific sequence V1753 (p = 0.002), which is associated with HCC (Tanaka, J Hepatol2006). The ROC curve of HBV DNA levels for HCC is shown. With the AUC of 0.508, there was no lower limit of HBV DNA level associated with lower chance of HCC. Conclusions: CP mutation was an independent risk factor for HCC. Its relationship with T I753 with respect to hepatocarcinogenesis needs further investigations. There was no HBVDNA level associated with lower risk for HCC.
Persistent Identifierhttp://hdl.handle.net/10722/102929
ISSN
2015 Impact Factor: 10.59
2015 SCImago Journal Rankings: 4.570

 

DC FieldValueLanguage
dc.contributor.authorYuen, RMFen_HK
dc.contributor.authorTanaka, Yen_HK
dc.contributor.authorShinkai, Nen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFung, JYYen_HK
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorYuen, JCHen_HK
dc.contributor.authorMizokami, Men_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2010-09-25T20:50:35Z-
dc.date.available2010-09-25T20:50:35Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 42nd Annual Meeting of the European Association for the Study of the Liver, Barcelona, Spain, 11-15 April 2007. In Journal of Hepatology, 2007, v. 46 n. S1, p. S184-S185 Abstract no. 485-
dc.identifier.issn0168-8278-
dc.identifier.urihttp://hdl.handle.net/10722/102929-
dc.description.abstractAims: To examine whether genotypesicore promoter (CP)/precore variants are independent risk factors for HCC and to define the low risk HBVDNA level in HCC. Patients and Methods: 248 HCC patients and 248 control patients matched for gender, age and HBeAg status were recruited. Results: Compared to controls, HCC patients had a higher prevalence of genotype C [57.4% vs 7 I .7% respectively, p = 0.00 I, O.R. I .9 (95% CT I .3-2.8)] and CP mutations [66.8% vs. 88.1% respectively, p i 0.001, O.R. 3.7 (95% CT 2.1-6.3)]. Prevalence of precore mutations was comparable between 2 groups. Multivariate analysis revealed CP mutations as the only independent risk factor for HCC (p i 0.001). CP mutations was associated with a specific sequence V1753 (p = 0.002), which is associated with HCC (Tanaka, J Hepatol2006). The ROC curve of HBV DNA levels for HCC is shown. With the AUC of 0.508, there was no lower limit of HBV DNA level associated with lower chance of HCC. Conclusions: CP mutation was an independent risk factor for HCC. Its relationship with T I753 with respect to hepatocarcinogenesis needs further investigations. There was no HBVDNA level associated with lower risk for HCC.-
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jhep-
dc.relation.ispartofJournal of Hepatologyen_HK
dc.titleRole of HBV genotypes, core promoter/precore mutations and HBV DNA levels on hepatocarcinogenesisen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailYuen, RMF: mfyuen@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFung, JYY: jfung@sicklehut.comen_HK
dc.identifier.emailWong, DKH: danywong@hku.hken_HK
dc.identifier.emailYuen, JCH: jchyuen@HKUCC.hku.hken_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, RMF=rp00479en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFung, JYY=rp00518en_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi0.1016/S0168-8278(07)62083-2-
dc.identifier.hkuros130870en_HK

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