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Article: Physical status of HPV-16 in esophageal squamous cell carcinoma

TitlePhysical status of HPV-16 in esophageal squamous cell carcinoma
Authors
KeywordsESCC
Esophageal cancer
esophageal squamous cell carcinoma
Esophageal squamous cell carcinoma
HPV
human papillomavirus
Human papillomavirus
Integration
opening reading frame
ORF
PCR
Physical status
polymerase chain reaction
Issue Date2005
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jcv
Citation
Journal Of Clinical Virology, 2005, v. 32 n. 1, p. 19-23 How to Cite?
AbstractBackground: Infection with high-risk human papillomavirus (HPV) has been implicated as one of the risk factors of esophageal squamous cell carcinoma (ESCC). Integration of viral DNA into host genome is essential for carcinogenesis since it promotes disruption of the HPV E2 gene, leading to abnormal expression of E6 and E7 oncoproteins. Objectives and study design: To investigate the viral integration status of HPV-16 infection in ESCC, 35 HPV-positive ESCC specimens collected from Chinese patients were subject to real-time quantitative PCR for determination of physical status of HPV-16 by analyzing the ratios of E2 to E6 genes. Results: Our results showed that only 8.6% (3/35) of the HPV-16 positive specimens harbored exclusively the episomal form (i.e. E2/E6 ratio ≥ 1), whereas the remaining 91.4% contained either only the integrated form (5.7%, with E2/E6 ratio = 0) or a mixture of episomal and integrated forms of viral molecules (85.7%, with E2/E6 ratios > 0 but <1). Amongst the 30 cancer specimens carrying mixed integrated and episomal forms, 28 had E2/integrated E6 ratios of less than 1, indicating a predominance of integrated form of viral genes in these lesions. Conclusion: Our finding of frequent integration of viral DNA in the host genome suggests that integration HPV-16 is common in ESCC from Chinese patients and implies that HPV infection may play a role in the pathogenesis of ESCC. © 2004 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67724
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 1.344
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSi, HXen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorPoon, CSPen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:57:41Z-
dc.date.available2010-09-06T05:57:41Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Clinical Virology, 2005, v. 32 n. 1, p. 19-23en_HK
dc.identifier.issn1386-6532en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67724-
dc.description.abstractBackground: Infection with high-risk human papillomavirus (HPV) has been implicated as one of the risk factors of esophageal squamous cell carcinoma (ESCC). Integration of viral DNA into host genome is essential for carcinogenesis since it promotes disruption of the HPV E2 gene, leading to abnormal expression of E6 and E7 oncoproteins. Objectives and study design: To investigate the viral integration status of HPV-16 infection in ESCC, 35 HPV-positive ESCC specimens collected from Chinese patients were subject to real-time quantitative PCR for determination of physical status of HPV-16 by analyzing the ratios of E2 to E6 genes. Results: Our results showed that only 8.6% (3/35) of the HPV-16 positive specimens harbored exclusively the episomal form (i.e. E2/E6 ratio ≥ 1), whereas the remaining 91.4% contained either only the integrated form (5.7%, with E2/E6 ratio = 0) or a mixture of episomal and integrated forms of viral molecules (85.7%, with E2/E6 ratios > 0 but <1). Amongst the 30 cancer specimens carrying mixed integrated and episomal forms, 28 had E2/integrated E6 ratios of less than 1, indicating a predominance of integrated form of viral genes in these lesions. Conclusion: Our finding of frequent integration of viral DNA in the host genome suggests that integration HPV-16 is common in ESCC from Chinese patients and implies that HPV infection may play a role in the pathogenesis of ESCC. © 2004 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/jcven_HK
dc.relation.ispartofJournal of Clinical Virologyen_HK
dc.rightsJournal of Clinical Virology. Copyright © Elsevier BV.en_HK
dc.subjectESCC-
dc.subjectEsophageal cancer-
dc.subjectesophageal squamous cell carcinoma-
dc.subjectEsophageal squamous cell carcinoma-
dc.subjectHPV-
dc.subjecthuman papillomavirus-
dc.subjectHuman papillomavirus-
dc.subjectIntegration-
dc.subjectopening reading frame-
dc.subjectORF-
dc.subjectPCR-
dc.subjectPhysical status-
dc.subjectpolymerase chain reaction-
dc.subject.meshCarcinoma, Squamous Cell - genetics - pathology - virologyen_HK
dc.subject.meshDNA-Binding Proteins - geneticsen_HK
dc.subject.meshEsophageal Neoplasms - genetics - pathology - virologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshOncogene Proteins, Viral - geneticsen_HK
dc.subject.meshPapillomaviridae - classification - genetics - isolation & purificationen_HK
dc.subject.meshPapillomavirus Infections - complicationsen_HK
dc.subject.meshRepressor Proteins - geneticsen_HK
dc.subject.meshVirus Integration - geneticsen_HK
dc.titlePhysical status of HPV-16 in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1386-6532&volume=32&spage=19&epage=23&date=2005&atitle=Physical+status+of+HPV-16+in+esophageal+squamous+cell+carcinomaen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jcv.2004.04.004en_HK
dc.identifier.pmid15572001-
dc.identifier.scopuseid_2-s2.0-9644258597en_HK
dc.identifier.hkuros96582en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9644258597&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue1en_HK
dc.identifier.spage19en_HK
dc.identifier.epage23en_HK
dc.identifier.isiWOS:000226189600003-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridSi, HX=36780537100en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridPoon, CSP=7202672697en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK
dc.identifier.issnl1386-6532-

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