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Epstein‐Barr virus infection and P53 expression in HIV‐related oral large B cell lymphoma
Author(s) -
Calzolari Anna,
Papucci Alessandra,
Baroni Gianna,
Ficarra Giuseppe,
Porfirio Berardino,
Chiarelli Ilaria,
Di Lollo Simonetta
Publication year - 1999
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/(sici)1097-0347(199908)21:5<454::aid-hed12>3.0.co;2-o
Subject(s) - biology , lymphoma , epstein–barr virus , exon , virus , gene , virology , single strand conformation polymorphism , in situ hybridization , gene expression , epstein–barr virus infection , microbiology and biotechnology , cancer research , immunology , genetics
Background Head and neck non‐Hodgkin's lymphomas in HIV positive patients are highly related with Epstein‐Barr virus (EBV) infection. In general, viral agents can alter p53 protein levels by enhancing degradation of cellular p53 or by increasing its half‐life by viral protein‐p53 interaction. Moreover, it has been reported that modifications of p53 gene can modulate tumor cells' response to radio‐ and chemotherapy. Methods To assess a possible role of EBV infection, p53 protein deregulation, and p53 gene alterations in exons 5 to 8, we have studied six cases of HIV‐related primary oral large B‐cell lymphoma. We used in situ hybridization (ISH) for EBV‐DNA and EBV‐encoded nuclear RNA‐1 (EBER‐1), immunohistochemistry (IHC) for EBV latent membrane protein ‐1 (LMP‐1) and p53 proteins expression, and single strand conformational polymorphism (SSCP) analysis to screen p53 gene mutations in exons 5 to 8. Results The EBV‐DNA was present in all specimens, according to conventional DNA‐ISH. No evidence for EBER‐1 was found by ISH. The presence of EBV‐DNA was correlated with the LMP‐1 expression in all but one case. Moreover, p53 protein expression was negative in three cases and strongly positive in the others. However, mutational analysis of p53 gene in exons 5–8 showed no alteration. Conclusions Our data may suggest that both EBV infection and LMP‐1 expression may cause p53 loss of function even in the absence of p53 gene mutations, as assessed by SSCP. We speculate that the presence of EBV‐infection and p53 protein deregulation may be responsible for radio‐ and chemotherapy resistance, by influencing apoptosis of cancer cells. © 1999 John Wiley & Sons, Inc. Head Neck 21: 454–460, 1999.