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Extensive analysis of duplicated-inverted hepatitis B virus integrations in human hepatocellular carcinoma.

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dc.contributor.authorPineau, P-
dc.contributor.authorMarchio, A-
dc.contributor.authorMattei, MG-
dc.contributor.authorKim, WH-
dc.contributor.authorYoun, JK-
dc.contributor.authorTiollais, P-
dc.contributor.authorDejean, A-
dc.date.accessioned2011-08-24T01:18:38Z-
dc.date.available2011-08-24T01:18:38Z-
dc.date.issued1998-
dc.identifier.issn0022-1317-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3911-
dc.description.abstractHepatitis B virus (HBV) DNA is found chromosomally integrated into the genome of the majority of hepatocellular carcinomas (HCC) arising in chronic HBV carriers suggesting that, in some instances, viral sequences may be directly responsible for oncogenic conversion. In an attempt to clarify the oncogenic potential of integrated HBV sequences, we performed an extensive analysis of two single integrations present in HCC which developed in non-cirrhotic livers from HBsAg-positive Korean patients. In both cases, integrated viral sequences were characterized by a duplicated-inverted configuration involving the flanking cellular sequences, a pattern consistently found in many amplicons isolated from mammalian cells. Integration sites are characterized by an AT-rich content and the presence of topoisomerase I and II cleavage target sequences as well as other recombination-prone motifs. The chromosomal locations of the integration sites were determined as 8q13 and 10q22 in the human genome, two regions known to harbour genes involved in tumorigenesis. The cis-activating potential of the integrations in their original configuration was also investigated in a transient transfection assay in HepG2 cells. Integrated sequences, rather than activating heterologous promoters, show either no activity or a weak tendency to inhibit activation of neighbouring reporter genes. The implications of our findings for the understanding of primary liver cancer development are discussed.-
dc.language.isoen-
dc.subject.MESHAdult-
dc.subject.MESHCarcinoma, Hepatocellular-
dc.subject.MESHChromosomes, Human, Pair 10-
dc.subject.MESHChromosomes, Human, Pair 8-
dc.subject.MESHDNA, Viral-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHHepatitis B virus-
dc.subject.MESHHumans-
dc.subject.MESHIn Situ Hybridization, Fluorescence-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHMolecular Sequence Data-
dc.subject.MESHRecombination, Genetic-
dc.subject.MESHTumor Cells, Cultured-
dc.subject.MESHVirus Integration-
dc.titleExtensive analysis of duplicated-inverted hepatitis B virus integrations in human hepatocellular carcinoma.-
dc.typeArticle-
dc.identifier.pmid9519839-
dc.identifier.urlhttp://vir.sgmjournals.org/cgi/pmidlookup?view=long&pmid=9519839-
dc.contributor.affiliatedAuthor윤, 정구-
dc.type.localJournal Papers-
dc.identifier.doi10.1099/0022-1317-79-3-591-
dc.citation.titleThe Journal of general virology-
dc.citation.volume79-
dc.citation.numberPt3-
dc.citation.date1998-
dc.citation.startPage591-
dc.citation.endPage600-
dc.identifier.bibliographicCitationThe Journal of general virology, 79(Pt3). : 591-600, 1998-
dc.identifier.eissn1465-2099-
dc.relation.journalidJ000221317-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
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