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Article: Risk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels

TitleRisk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levels
Authors
Issue Date2008
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2008, v. 57 n. 1, p. 98-102 How to Cite?
Abstract
Background/aim: To examine the risks for hepatocellular carcinoma (HCC) with respect to hepatitis B virus (HBV) genotypes, specific viral mutations (MT), serum HBV DNA levels, and cirrhosis. Methods: HBV genotypes, 1653/1753/core promoter (CP)/precore MT and HBV DNA levels were determined in 248 HBV patients with HCC and 248 HBV controls. Results: Genotype C, CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis had a higher risk for HCC compared to patients with genotype B (p = 0.001, OR 1.9), CP wild-type (WT) (p<0.001, OR 4.1), C1653 (p = 0.028, OR 2.4), HBV DNA <4 log 10 copies/ml (p = 0.003, OR 2.1) and without cirrhosis (p<0.001, OR 4.0) respectively. Multivariate analysis showed that CP-MT, T1653, HBV DNA ≥4 log 10 copies/ml and cirrhosis were independent factors for HCC (all p<0.05). A receiver operating characteristics curve showed no cut-off HBV DNA level associated with minimal chance of HCC. Patients with CP-MT and cirrhosis had a 22.2-fold increased risk of HCC compared to patients with CP-WT and without cirrhosis. Patients with CP-MT and HBV DNA levels ≥4 log 10 copies/ml had a 7.2-fold increased risk of HCC compared to patients with CP-WT and HBV DNA levels <4 log 10 copies/ml. Patients with CP-MT and T1653 had a 9.9-fold increased risk of HCC compared to patients with wild-type for both regions. Conclusions: CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis are independent factors for development of HCC. The risks increased substantially in patients having these factors in combination.
Persistent Identifierhttp://hdl.handle.net/10722/57531
ISSN
2013 Impact Factor: 13.319
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorTanaka, Yen_HK
dc.contributor.authorShinkai, Nen_HK
dc.contributor.authorPoon, RTen_HK
dc.contributor.authorBut, DYKen_HK
dc.contributor.authorFong, DYTen_HK
dc.contributor.authorFung, Jen_HK
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorYuen, JCHen_HK
dc.contributor.authorMizokami, Men_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2010-04-12T01:39:15Z-
dc.date.available2010-04-12T01:39:15Z-
dc.date.issued2008en_HK
dc.identifier.citationGut, 2008, v. 57 n. 1, p. 98-102en_HK
dc.identifier.issn0017-5749en_HK
dc.identifier.urihttp://hdl.handle.net/10722/57531-
dc.description.abstractBackground/aim: To examine the risks for hepatocellular carcinoma (HCC) with respect to hepatitis B virus (HBV) genotypes, specific viral mutations (MT), serum HBV DNA levels, and cirrhosis. Methods: HBV genotypes, 1653/1753/core promoter (CP)/precore MT and HBV DNA levels were determined in 248 HBV patients with HCC and 248 HBV controls. Results: Genotype C, CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis had a higher risk for HCC compared to patients with genotype B (p = 0.001, OR 1.9), CP wild-type (WT) (p<0.001, OR 4.1), C1653 (p = 0.028, OR 2.4), HBV DNA <4 log 10 copies/ml (p = 0.003, OR 2.1) and without cirrhosis (p<0.001, OR 4.0) respectively. Multivariate analysis showed that CP-MT, T1653, HBV DNA ≥4 log 10 copies/ml and cirrhosis were independent factors for HCC (all p<0.05). A receiver operating characteristics curve showed no cut-off HBV DNA level associated with minimal chance of HCC. Patients with CP-MT and cirrhosis had a 22.2-fold increased risk of HCC compared to patients with CP-WT and without cirrhosis. Patients with CP-MT and HBV DNA levels ≥4 log 10 copies/ml had a 7.2-fold increased risk of HCC compared to patients with CP-WT and HBV DNA levels <4 log 10 copies/ml. Patients with CP-MT and T1653 had a 9.9-fold increased risk of HCC compared to patients with wild-type for both regions. Conclusions: CP-MT, T1653, HBV DNA levels ≥4 log 10 copies/ml and cirrhosis are independent factors for development of HCC. The risks increased substantially in patients having these factors in combination.en_HK
dc.languageengen_HK
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/en_HK
dc.relation.ispartofGuten_HK
dc.rightsGut. Copyright © B M J Publishing Group.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCarcinoma, Hepatocellular - virologyen_HK
dc.subject.meshEnhancer Elements (Genetics) - geneticsen_HK
dc.subject.meshHepatitis B virus - geneticsen_HK
dc.subject.meshLiver Neoplasms - virologyen_HK
dc.subject.meshPromoter Regions (Genetics) - geneticsen_HK
dc.titleRisk for hepatocellular carcinoma with respect to hepatitis B virus genotypes B/C, specific mutations of enhancer II/core promoter/precore regions and HBV DNA levelsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0017-5749&volume=57&issue=1&spage=98&epage=102&date=2008&atitle=Risk+for+hepatocellular+carcinoma+with+respect+to+hepatitis+B+virus+genotypes+B/C,+specific+mutations+of+enhancer+II/core+promoter/precore+regions+and+HBV+DNA+levelsen_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.emailPoon, RT: poontp@hku.hken_HK
dc.identifier.emailFong, DYT: dytfong@hku.hken_HK
dc.identifier.emailFung, J: jfung@sicklehut.comen_HK
dc.identifier.emailWong, DKH: danywong@hku.hken_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityPoon, RT=rp00446en_HK
dc.identifier.authorityFong, DYT=rp00253en_HK
dc.identifier.authorityFung, J=rp00518en_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1136/gut.2007.119859en_HK
dc.identifier.pmid17483190en_HK
dc.identifier.scopuseid_2-s2.0-38349138512en_HK
dc.identifier.hkuros130659-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38349138512&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume57en_HK
dc.identifier.issue1en_HK
dc.identifier.spage98en_HK
dc.identifier.epage102en_HK
dc.identifier.isiWOS:000251778400021-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridTanaka, Y=7405315865en_HK
dc.identifier.scopusauthoridShinkai, N=7003826116en_HK
dc.identifier.scopusauthoridPoon, RT=7103097223en_HK
dc.identifier.scopusauthoridBut, DYK=24343113400en_HK
dc.identifier.scopusauthoridFong, DYT=35261710300en_HK
dc.identifier.scopusauthoridFung, J=23091109300en_HK
dc.identifier.scopusauthoridWong, DKH=7401535819en_HK
dc.identifier.scopusauthoridYuen, JCH=7102620480en_HK
dc.identifier.scopusauthoridMizokami, M=7103318255en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK

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