Association of p53 and bcl-2 expression with Epstein-Barr virus infection in the cancers of head and neck

Citation
Hj. Yang et al., Association of p53 and bcl-2 expression with Epstein-Barr virus infection in the cancers of head and neck, HEAD NECK, 23(8), 2001, pp. 629-636
Citations number
33
Categorie Soggetti
Otolaryngology
Journal title
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK
ISSN journal
10433074 → ACNP
Volume
23
Issue
8
Year of publication
2001
Pages
629 - 636
Database
ISI
SICI code
1043-3074(200108)23:8<629:AOPABE>2.0.ZU;2-J
Abstract
Background. Reports that have both evaluated the site-specific Epstein-Barr virus (EBV) infection and compared it with the expression of the EBV-relat ed proto-oncogenes and tumor suppressor genes in the various cancers of hea d and neck are scarce. Methods. Thirty-eight nasopharyngeal carcinoma (NPC) cases, 32 oropharyngea l or hypopharyngeal carcinoma (OPC/HPC) cases, and 93 laryngeal carcinoma ( LC) cases were evaluated with in situ hybridization on EBV-encoded small RN A (EBER) and immunohistochemical assessments of the p53, bcl-2, and epiderm al growth factor receptor (EGFR) by use of formalin-fixed paraffin-embedded tissue array slides. Results. The expression of viral EBERs was observed in more than two thirds (71.1%) of the NPC cases. In contrast, only 1 case of OPC and none of the HPC or LC cases exhibited EBV positivity. in the nonkeratinizing NPC, the E BV positivity was significantly associated with both frequent p53 overexpre ssion (p = .033) and bcl-2 expression (p = .001). In the EBV-positive nonke ratinizing NPC, a correlation between p53 overexpression and the tumor infi ltration lymphocyte (TIL) density was noted (P = .012). Conclusions. A site-specific expression of viral EBER was demonstrated in t he head and neck cancers, which suggests an important role for both p53 and bcl-2 in the carcinogenesis of an EBV-infected NPC. The correlation betwee n p53 overexpression and the TIL density in the EBV-infected NPC suggests t hat the product of a lymphoepithelial interaction, such as A20, can induce a dysfunctional p53 protein. (C) 2001 John Wiley & Sons, Inc.