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Review
. 2000 Oct;53(5):248-54.
doi: 10.1136/mp.53.5.248.

Epstein-Barr virus infection in the pathogenesis of nasopharyngeal carcinoma

Affiliations
Review

Epstein-Barr virus infection in the pathogenesis of nasopharyngeal carcinoma

G Niedobitek. Mol Pathol. 2000 Oct.

Abstract

The association of nasopharyngeal carcinoma (NPC) with the Epstein-Barr virus (EBV) was firmly established as early as 1973. Nevertheless, the role for the virus in the pathogenesis of NPC is still controversial. In this article, the evidence implicating EBV in the development of NPC is reviewed, focusing on the cellular site of EBV persistence, the association of the virus with different NPC histotypes, the tumour cell phenotype in the context of viral latent gene expression, and the possible role of the lymphoid stroma.

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Figures

Figure 1
Figure 1
(A) Double labelling in situ hybridisation and immunohistochemistry reveals expression of the Epstein-Barr virus (EBV) encoded RNAs (EBERs) (black grains) in virtually all cytokeratin positive (red labelling) tumour cells of an undifferentiated nasopharyngeal carcinoma. (B) Detection of latent membrane protein 2A (LMP2A) by immunohistochemistry in an Epstein-Barr virus positive undifferentiated carcinoma (see text).
Figure 2
Figure 2
Possible interactions between tumour cells and tumour infiltrating lymphocytes in Hodgkin's disease (left) and undifferentiated nasopharyngeal carcinoma (right, modified and extended from Gruss and colleagues77). IL, interleukin; TARC, thymus and activation regulated chemokine.

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