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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
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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
 
AuthorsYuen, MF2 2
Tanaka, Y1
Shinkai, N1
Poon, RT2
But, DYK2
Fong, DYT2
Fung, J2
Wong, DKH2
Yuen, JCH2
Mizokami, M1
Lai, CL2
 
Issue Date2008
 
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
CitationGut, 2008, v. 57 n. 1, p. 98-102 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gut.2007.119859
 
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.
 
ISSN0017-5749
2012 Impact Factor: 10.732
2012 SCImago Journal Rankings: 3.379
 
DOIhttp://dx.doi.org/10.1136/gut.2007.119859
 
ISI Accession Number IDWOS:000251778400021
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorYuen, MF
 
dc.contributor.authorTanaka, Y
 
dc.contributor.authorShinkai, N
 
dc.contributor.authorPoon, RT
 
dc.contributor.authorBut, DYK
 
dc.contributor.authorFong, DYT
 
dc.contributor.authorFung, J
 
dc.contributor.authorWong, DKH
 
dc.contributor.authorYuen, JCH
 
dc.contributor.authorMizokami, M
 
dc.contributor.authorLai, CL
 
dc.date.accessioned2010-04-12T01:39:15Z
 
dc.date.available2010-04-12T01:39:15Z
 
dc.date.issued2008
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationGut, 2008, v. 57 n. 1, p. 98-102 [How to Cite?]
DOI: http://dx.doi.org/10.1136/gut.2007.119859
 
dc.identifier.doihttp://dx.doi.org/10.1136/gut.2007.119859
 
dc.identifier.epage102
 
dc.identifier.hkuros130659
 
dc.identifier.isiWOS:000251778400021
 
dc.identifier.issn0017-5749
2012 Impact Factor: 10.732
2012 SCImago Journal Rankings: 3.379
 
dc.identifier.issue1
 
dc.identifier.openurl
 
dc.identifier.pmid17483190
 
dc.identifier.scopuseid_2-s2.0-38349138512
 
dc.identifier.spage98
 
dc.identifier.urihttp://hdl.handle.net/10722/57531
 
dc.identifier.volume57
 
dc.languageeng
 
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofGut
 
dc.relation.referencesReferences in Scopus
 
dc.rightsGut. Copyright © B M J Publishing Group.
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshCarcinoma, Hepatocellular - virology
 
dc.subject.meshEnhancer Elements (Genetics) - genetics
 
dc.subject.meshHepatitis B virus - genetics
 
dc.subject.meshLiver Neoplasms - virology
 
dc.subject.meshPromoter Regions (Genetics) - genetics
 
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 levels
 
dc.typeArticle
 
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<contributor.author>Tanaka, Y</contributor.author>
<contributor.author>Shinkai, N</contributor.author>
<contributor.author>Poon, RT</contributor.author>
<contributor.author>But, DYK</contributor.author>
<contributor.author>Fong, DYT</contributor.author>
<contributor.author>Fung, J</contributor.author>
<contributor.author>Wong, DKH</contributor.author>
<contributor.author>Yuen, JCH</contributor.author>
<contributor.author>Mizokami, M</contributor.author>
<contributor.author>Lai, CL</contributor.author>
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<description.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 &#8805;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&lt;0.001, OR 4.1), C1653 (p = 0.028, OR 2.4), HBV DNA &lt;4 log 10 copies/ml (p = 0.003, OR 2.1) and without cirrhosis (p&lt;0.001, OR 4.0) respectively. Multivariate analysis showed that CP-MT, T1653, HBV DNA &#8805;4 log 10 copies/ml and cirrhosis were independent factors for HCC (all p&lt;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 &#8805;4 log 10 copies/ml had a 7.2-fold increased risk of HCC compared to patients with CP-WT and HBV DNA levels &lt;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 &#8805;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.</description.abstract>
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<subject.mesh>Carcinoma, Hepatocellular - virology</subject.mesh>
<subject.mesh>Enhancer Elements (Genetics) - genetics</subject.mesh>
<subject.mesh>Hepatitis B virus - genetics</subject.mesh>
<subject.mesh>Liver Neoplasms - virology</subject.mesh>
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Author Affiliations
  1. Nagoya City University
  2. The University of Hong Kong