Epstein–Barr virus infection in colorectal neoplasms associated with inflammatory bowel disease: detection of the virus in lymphomas but not in adenocarcinomas
- 16 July 2003
- journal article
- research article
- Published by Wiley in The Journal of Pathology
- Vol. 201 (2) , 312-318
Abstract
Epstein–Barr virus (EBV) is associated with several lymphoid and epithelial human malignancies. The latter include gastric adenocarcinomas, while sporadic colorectal adenocarcinomas (CRCs) have been reported to be EBV‐negative. Recently, increased numbers of EBV‐infected B lymphocytes have been detected in intestinal mucosal samples affected by ulcerative colitis (UC) and, to a lesser extent, Crohn's disease (CD). Both CRC and colorectal non‐Hodgkin's lymphoma (NHL) are recognized complications of inflammatory bowel disease (IBD), but it is unclear to what extent EBV contributes to the development of these neoplasms. Seventeen cases of IBD‐associated CRC and nine cases of IBD‐associated colorectal NHL were therefore studied for the presence of EBV by in situ hybridization. EBV‐positive cases were further studied for the expression of the EBV‐encoded nuclear antigen (EBNA) 2 and the latent membrane protein (LMP) 1 of EBV by immunohistochemistry. Four out of seven cases of colorectal NHL associated with UC were shown to be EBV‐positive. In addition, two of two colorectal NHLs developing in patients with CD were EBV‐positive. Of the EBV‐positive lymphomas, three displayed a pattern of EBV latent gene expression consistent with type I latency (EBNA2 − /LMP1 − ), two a type II pattern (EBNA2 − /LMP1 + ), and one a type III pattern (EBNA2 + /LMP1 + ). These findings suggest that EBV infection is involved in the pathogenesis of a proportion of colorectal NHLs developing in IBD. Iatrogenic immunosuppression may contribute to the development of these lymphomas. By contrast, all 17 IBD‐associated CRCs were EBV‐negative, including a case of CRC occurring synchronously with an EBV‐positive NHL. In conjunction with previous reports on sporadic CRCs, this suggests that EBV is not involved in the pathogenesis of CRC. Copyright © 2003 John Wiley & Sons, Ltd.Keywords
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