Abstract 4784: Genetic alterations in premalignant nasopharyngeal epithelium support stable EBV infection
EBV 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...
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Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2013-04, Vol.73 (8_Supplement), p.4784-4784 |
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Sprache: | eng |
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Zusammenfassung: | EBV 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 resistance to differentiation induction in immortalized nasopharyngeal epithelial cells. EBV infection is closely associated with undifferentiated nasopharyngeal carcinoma. We observed that cyclin D1 overexpression is common in premalignant nasopharyngeal epithelium and co-exist with EBV infection shown by EBER staining. All these showed that cyclin D1 overexpression or suppression of the p16 activation support EBV infection establishment in premalignant nasopharyngeal epithelium which has been postulated to be an important and early event in NPC development.
Citation Format: George Sai-Wah Tsao, Anna CM Tsang, Elaine YL Yip, W Deng, Annie LM Cheung, KW Lo. Genetic alterations in premalignant nasopharyngeal epithelium support stable EBV infection. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4784. doi:10.1158/1538-7445.AM2013-4784
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend. |
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ISSN: | 0008-5472 1538-7445 |
DOI: | 10.1158/1538-7445.AM2013-4784 |