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Conference Paper: Genetic alterations in premalignant nasopharyngeal epithelium support stable EBV infection

TitleGenetic alterations in premalignant nasopharyngeal epithelium support stable EBV infection
Authors
Tsao, GSWTsang, ACMYip, EYLDeng, WCheung, ALMLo, KW
KeywordsMedical sciences
Oncology
Issue Date2013
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 104th Annual Meeting of the American Association for Cancer Research (AACR 2013), Washington, DC, PA., 6-10 April 2013. In Cancer Research, 2013, v. 73 n. 8, suppl. 1, abstract no. 4784 How to Cite?
DOI: http://dx.doi.org/10.1158/1538-7445.AM2013-4784
AbstractEBV infection is closely associated with nasopharyngeal carcinoma. Early events involved in the establishment of EBV infection in premalignant nasopharyngeal epithelium are largely undefined. We have established multiple immortalized nasopharygeal epithelial cells as premalignant cell models for EBV infection. We observed that nasopharyngeal epithelial cells immortalized by combined actions of telomerase and cyclin D1 or knocking down p16 could support stable EBV infection. Furthermore, we observed that EBV infection commonly induces growth inhibition and senescence in infected nasopharyngeal epithelial cells. Overexpression of cyclin D1 suppresses the growth inhibition and support EBV infection. Furthermore cyclin D1 expression confers ...
DescriptionPoster Presentations - Transformation and Promotion: abstract no. 4784
Persistent Identifierhttp://hdl.handle.net/10722/186566
ISSN
0008-5472
2021 Impact Factor: 13.312
2020 SCImago Journal Rankings: 4.103
ISI Accession Number ID
WOS:000331220604346

 

DC FieldValueLanguage
dc.contributor.authorTsao, GSWen_US
dc.contributor.authorTsang, ACMen_US
dc.contributor.authorYip, EYLen_US
dc.contributor.authorDeng, Wen_US
dc.contributor.authorCheung, ALMen_US
dc.contributor.authorLo, KWen_US
dc.date.accessioned2013-08-20T12:13:28Z-
dc.date.available2013-08-20T12:13:28Z-
dc.date.issued2013en_US
dc.identifier.citationThe 104th Annual Meeting of the American Association for Cancer Research (AACR 2013), Washington, DC, PA., 6-10 April 2013. In Cancer Research, 2013, v. 73 n. 8, suppl. 1, abstract no. 4784en_US
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/186566-
dc.descriptionPoster Presentations - Transformation and Promotion: abstract no. 4784-
dc.description.abstractEBV infection is closely associated with nasopharyngeal carcinoma. Early events involved in the establishment of EBV infection in premalignant nasopharyngeal epithelium are largely undefined. We have established multiple immortalized nasopharygeal epithelial cells as premalignant cell models for EBV infection. We observed that nasopharyngeal epithelial cells immortalized by combined actions of telomerase and cyclin D1 or knocking down p16 could support stable EBV infection. Furthermore, we observed that EBV infection commonly induces growth inhibition and senescence in infected nasopharyngeal epithelial cells. Overexpression of cyclin D1 suppresses the growth inhibition and support EBV infection. Furthermore cyclin D1 expression confers ...-
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Researchen_US
dc.subjectMedical sciences-
dc.subjectOncology-
dc.titleGenetic alterations in premalignant nasopharyngeal epithelium support stable EBV infectionen_US
dc.typeConference_Paperen_US
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_US
dc.identifier.emailTsang, ACM: annatsan@hku.hken_US
dc.identifier.emailYip, EYL: yimling@hkucc.hku.hken_US
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_US
dc.identifier.emailCheung, ALM: lmcheung@hku.hken_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.identifier.authorityDeng, W=rp01640en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1538-7445.AM2013-4784-
dc.identifier.hkuros217527en_US
dc.identifier.volume73-
dc.identifier.issue8, suppl. 1-
dc.identifier.isiWOS:000331220604346-
dc.publisher.placeUnited States-
dc.identifier.issnl0008-5472-

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