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Article: The role of Epstein-Barr virus in epithelial malignancies

TitleThe role of Epstein-Barr virus in epithelial malignancies
Authors
Issue Date2015
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal of Pathology, 2015, v. 235 n. 2, p. 323-333 How to Cite?
AbstractThe close association of Epstein-Barr virus (EBV) infection with non-keratinizing nasopharyngeal carcinomas and a subset of gastric carcinomas suggests that EBV infection is a crucial event in these cancers. The difficulties encountered in infecting and transforming primary epithelial cells in experimental systems suggest that the role of EBV in epithelial malignancies is complex and multifactorial in nature. Genetic alterations in the premalignant epithelium may support the establishment of latent EBV infection, which is believed to be an initiation event. Oncogenic properties have been reported in multiple EBV latent genes. The BamH1 A rightwards transcripts (BART s) and the BART -encoded microRNAs (miR-BART s) are highly expressed in EBV-associated epithelial malignancies and may induce malignant transformation. However, enhanced proliferation may not be the crucial function of EBV infection in epithelial malignancies, at least in the early stages of cancer development. EBV-encoded gene products may confer anti-apoptotic properties and promote the survival of infected premalignant epithelial cells harbouring genetic alterations. Multiple EBV-encoded microRNAs have been reported to have immune evasion functions. Genetic alterations in host cells, as well as inflammatory stroma, could modulate the expression of EBV genes and alter the growth properties of infected premalignant epithelial cells, encouraging their selection during carcinogenesis. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/220088
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTsao, GSW-
dc.contributor.authorTsang, CM-
dc.contributor.authorTo, KF-
dc.contributor.authorLo, KW-
dc.date.accessioned2015-10-16T06:28:45Z-
dc.date.available2015-10-16T06:28:45Z-
dc.date.issued2015-
dc.identifier.citationJournal of Pathology, 2015, v. 235 n. 2, p. 323-333-
dc.identifier.issn0022-3417-
dc.identifier.urihttp://hdl.handle.net/10722/220088-
dc.description.abstractThe close association of Epstein-Barr virus (EBV) infection with non-keratinizing nasopharyngeal carcinomas and a subset of gastric carcinomas suggests that EBV infection is a crucial event in these cancers. The difficulties encountered in infecting and transforming primary epithelial cells in experimental systems suggest that the role of EBV in epithelial malignancies is complex and multifactorial in nature. Genetic alterations in the premalignant epithelium may support the establishment of latent EBV infection, which is believed to be an initiation event. Oncogenic properties have been reported in multiple EBV latent genes. The BamH1 A rightwards transcripts (BART s) and the BART -encoded microRNAs (miR-BART s) are highly expressed in EBV-associated epithelial malignancies and may induce malignant transformation. However, enhanced proliferation may not be the crucial function of EBV infection in epithelial malignancies, at least in the early stages of cancer development. EBV-encoded gene products may confer anti-apoptotic properties and promote the survival of infected premalignant epithelial cells harbouring genetic alterations. Multiple EBV-encoded microRNAs have been reported to have immune evasion functions. Genetic alterations in host cells, as well as inflammatory stroma, could modulate the expression of EBV genes and alter the growth properties of infected premalignant epithelial cells, encouraging their selection during carcinogenesis. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.-
dc.languageeng-
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130-
dc.relation.ispartofJournal of Pathology-
dc.rightsJournal of Pathology. Copyright © John Wiley & Sons.-
dc.rightsSpecial Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)-
dc.titleThe role of Epstein-Barr virus in epithelial malignancies-
dc.typeArticle-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailTsang, CM: annatsan@hku.hk-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityTsang, CM=rp01964-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/path.4448-
dc.identifier.pmid25251730-
dc.identifier.pmcidPMC4280676-
dc.identifier.scopuseid_2-s2.0-84917705494-
dc.identifier.hkuros255641-
dc.identifier.volume235-
dc.identifier.issue2-
dc.identifier.spage323-
dc.identifier.epage333-
dc.identifier.isiWOS:000346190300016-
dc.publisher.placeUnited Kingdom-

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