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Specific mutations in the enhancer II/core promoter/precore regions of hepatitis B virus subgenotype C2 in Korean patients with hepatocellular carcinoma.

DC Field Value Language
dc.contributor.author전재윤-
dc.contributor.author한광협-
dc.contributor.author김도영-
dc.contributor.author김자경-
dc.contributor.author박준용-
dc.contributor.author안상훈-
dc.contributor.author윤영준-
dc.contributor.author이중민-
dc.date.accessioned2015-04-24T16:38:06Z-
dc.date.available2015-04-24T16:38:06Z-
dc.date.issued2009-
dc.identifier.issn0146-6615-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/103884-
dc.description.abstractRecently, hepatitis B virus (HBV) genotypes and mutations have been reported to be related to hepatocellular carcinoma (HCC). This cross-sectional case-control study examined the relationship between HCC and mutations in the enhancer II/core promoter and precore regions of HBV by comparing 135 Korean HCC patients infected with HBV genotype C2 (HBV/C2; HCC group) with 135 age-, sex-, and hepatitis B e antigen (HBeAg) status-matched patients without HCC (non- HCC group). Age and sex were also matched between HBeAg-positive and -negative patients. The prevalence of T1653, A1689, V1753, T1762/A1764, T1846, A1850, C1858, and A1896 mutations was evaluated in this population. The prevalence of the T1653 mutation in the box alpha region, the T1689 [corrected] mutation in between the box alpha and beta regions, and the T1762/A1764 mutations in the basal core promoter region was significantly higher in the HCC group compared to the non-HCC group (8.9% vs. 2.2%, P = 0.017; 19.3% vs. 4.4%, P < 0.001; and 60.7% vs. 22.2%; P < 0.001). Among HBeAg-negative patients, the frequency of the T1653 mutation was higher in the HCC group. Regardless of HBeAg status, the prevalence of the T1689, [corrected] and T1762/A1764 mutations was higher in the HCC group than in the non-HCC group. However, no association was observed between mutations in the precore region and HCC. Upon multivariate analysis, the presence of the T1653, T1689, [corrected] and T1762/A1764 mutations was an independent predictive factor for HCC. The addition of the T1653 or T1689 [corrected] mutation to T1762/A1764 increased the risk of HCC. In conclusion, the T1653, T1689, [corrected] and/or T1762/A1764 mutations were associated with the development of HCC in Korean patients infected with HBV/C2.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1002~1008-
dc.relation.isPartOfJOURNAL OF MEDICAL VIROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHCarcinoma, Hepatocellular/virology*-
dc.subject.MESHCase-Control Studies-
dc.subject.MESHCross-Sectional Studies-
dc.subject.MESHDNA, Viral/genetics-
dc.subject.MESHFemale-
dc.subject.MESHHepatitis B Core Antigens/genetics*-
dc.subject.MESHHepatitis B virus/genetics*-
dc.subject.MESHHepatitis B virus/isolation & purification-
dc.subject.MESHHepatitis B, Chronic/complications*-
dc.subject.MESHHepatitis B, Chronic/virology*-
dc.subject.MESHHumans-
dc.subject.MESHKorea-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHPoint Mutation*-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHTrans-Activators/genetics*-
dc.subject.MESHViral Regulatory and Accessory Proteins/genetics*-
dc.titleSpecific mutations in the enhancer II/core promoter/precore regions of hepatitis B virus subgenotype C2 in Korean patients with hepatocellular carcinoma.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJa Kyung Kim-
dc.contributor.googleauthorHye Young Chang-
dc.contributor.googleauthorJung Min Lee-
dc.contributor.googleauthorOidov Baatarkhuu-
dc.contributor.googleauthorYoung Joon Yoon-
dc.contributor.googleauthorJun Yong Park-
dc.contributor.googleauthorDo Young Kim-
dc.contributor.googleauthorKwang-Hyub Han-
dc.contributor.googleauthorChae Yoon Chon-
dc.contributor.googleauthorSang Hoon Ahn-
dc.identifier.doi10.1002/jmv.21501-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA04268-
dc.contributor.localIdA00852-
dc.contributor.localIdA01675-
dc.contributor.localIdA02226-
dc.contributor.localIdA02582-
dc.contributor.localIdA03184-
dc.contributor.localIdA03544-
dc.contributor.localIdA00385-
dc.relation.journalcodeJ01587-
dc.identifier.eissn1096-9071-
dc.identifier.pmid19382267-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1002/jmv.21501/abstract-
dc.subject.keywordhepatitis B virus-
dc.subject.keywordhepatitis B virus X protein-
dc.subject.keywordhepatocellular carcinoma-
dc.subject.keywordmutation-
dc.subject.keywordoncogenic viruses-
dc.contributor.alternativeNameChon, Chae Yoon-
dc.contributor.alternativeNameHan, Kwang Hyup-
dc.contributor.alternativeNameKim, Do Young-
dc.contributor.alternativeNameKim, Ja Kyung-
dc.contributor.alternativeNamePark, Jun Yong-
dc.contributor.alternativeNameAhn, Sang Hoon-
dc.contributor.alternativeNameYoon, Young Joon-
dc.contributor.alternativeNameLee, Jung Min-
dc.contributor.affiliatedAuthorHan, Kwang Hyup-
dc.contributor.affiliatedAuthorKim, Ja Kyung-
dc.contributor.affiliatedAuthorPark, Jun Yong-
dc.contributor.affiliatedAuthorAhn, Sang Hoon-
dc.contributor.affiliatedAuthorYoon, Young Joon-
dc.contributor.affiliatedAuthorLee, Jung Min-
dc.contributor.affiliatedAuthorChon, Chae Yoon-
dc.contributor.affiliatedAuthorKim, Do Young-
dc.citation.volume81-
dc.citation.number6-
dc.citation.startPage1002-
dc.citation.endPage1008-
dc.identifier.bibliographicCitationJOURNAL OF MEDICAL VIROLOGY, Vol.81(6) : 1002-1008, 2009-
dc.identifier.rimsid37857-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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