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Article: Characterization of HBV integrants in 14 hepatocellular carcinomas: Association of truncated X gene and hepatocellular carcinogenesis

TitleCharacterization of HBV integrants in 14 hepatocellular carcinomas: Association of truncated X gene and hepatocellular carcinogenesis
Authors
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2004, v. 23 n. 1, p. 142-148 How to Cite?
AbstractAlthough the integration of hepatitis B virus (HBV) into human DNA has been found to be associated with the development of hepatocellular carcinoma (HCC), the molecular mechanism remains unclear. In order to obtain additional insight into the correlation of HBV integration and HCC development, integrated HBV in 14 primary HCC cases was isolated and characterized by sequencing analysis. Our findings in this study showed that: (1) none of the known cellular oncogene or tumor suppressor gene was affected by the HBV integration; (2) although the integration of HBV is random, the integration site was often within or close to human repetitive sequences; (3) integrated HBV may possess the capacity to transpose to another chromosome region through reintegration; (4) rearrangements of HBV sequence were observed in all the 14 integrants, involving (most frequently) X (12/14 integrants), P (8/14), S (7/14), and C (7/14) genes; and (5) 3′-deleted X gene and consequent C-terminal truncated X protein caused by HBV integration was observed in 10 cases. These deletions cause the losses of p53-dependent transcriptional repression binding site, transcription factor Sp1 binding site, and growth-suppressive effect domain, leading to cell proliferation and transformation. This finding suggests that 3′-deleted X gene caused by the HBV integration may play an important role in the HCC development.
Persistent Identifierhttp://hdl.handle.net/10722/71939
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLau, SHen_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorWu, MCen_HK
dc.contributor.authorWang, Ten_HK
dc.contributor.authorGuan, XYen_HK
dc.date.accessioned2010-09-06T06:36:42Z-
dc.date.available2010-09-06T06:36:42Z-
dc.date.issued2004en_HK
dc.identifier.citationOncogene, 2004, v. 23 n. 1, p. 142-148en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71939-
dc.description.abstractAlthough the integration of hepatitis B virus (HBV) into human DNA has been found to be associated with the development of hepatocellular carcinoma (HCC), the molecular mechanism remains unclear. In order to obtain additional insight into the correlation of HBV integration and HCC development, integrated HBV in 14 primary HCC cases was isolated and characterized by sequencing analysis. Our findings in this study showed that: (1) none of the known cellular oncogene or tumor suppressor gene was affected by the HBV integration; (2) although the integration of HBV is random, the integration site was often within or close to human repetitive sequences; (3) integrated HBV may possess the capacity to transpose to another chromosome region through reintegration; (4) rearrangements of HBV sequence were observed in all the 14 integrants, involving (most frequently) X (12/14 integrants), P (8/14), S (7/14), and C (7/14) genes; and (5) 3′-deleted X gene and consequent C-terminal truncated X protein caused by HBV integration was observed in 10 cases. These deletions cause the losses of p53-dependent transcriptional repression binding site, transcription factor Sp1 binding site, and growth-suppressive effect domain, leading to cell proliferation and transformation. This finding suggests that 3′-deleted X gene caused by the HBV integration may play an important role in the HCC development.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCarcinoma, Hepatocellular - virologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Rearrangementen_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.meshMolecular Sequence Dataen_HK
dc.subject.meshTrans-Activators - chemistry - geneticsen_HK
dc.subject.meshVirus Integrationen_HK
dc.titleCharacterization of HBV integrants in 14 hepatocellular carcinomas: Association of truncated X gene and hepatocellular carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=23&spage=142&epage=148&date=2004&atitle=Characterization+of+HBV+integrants+in+14+hepatocellular+carcinomas:+Association+of+truncated+X+gene+and+hepatocellular+carcinogenesis.en_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.onc.1206889en_HK
dc.identifier.pmid14712219-
dc.identifier.scopuseid_2-s2.0-0942289920en_HK
dc.identifier.hkuros96092en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0942289920&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue1en_HK
dc.identifier.spage142en_HK
dc.identifier.epage148en_HK
dc.identifier.isiWOS:000187895300015-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, Y=7601486269en_HK
dc.identifier.scopusauthoridLau, SH=7401596190en_HK
dc.identifier.scopusauthoridSham, JST=24472255400en_HK
dc.identifier.scopusauthoridWu, MC=7405593399en_HK
dc.identifier.scopusauthoridWang, T=36079778200en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK

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