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Expression of the recombination activating genes (RAG1 and RAG2) is not detectable in Epstein‐Barr virus‐associated human lymphomas
Author(s) -
Meru Nadine,
Jung Andreas,
Lisner Renate,
Niedobitek Gerald
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(200102)9999:9999<::aid-ijc1163>3.0.co;2-m
Subject(s) - rag2 , recombination activating gene , biology , lymphoma , epstein–barr virus , follicular lymphoma , virus , in situ hybridization , chromosomal translocation , gene , gammaherpesvirinae , gene expression , virology , cancer research , microbiology and biotechnology , immunology , herpesviridae , genetics , recombination , viral disease
The expression of the recombination activating genes (RAG1 and RAG2) is largely restricted to immature lymphoid cells. Previous studies have suggested that Epstein‐Barr virus (EBV) infection may lead to a re‐induction of RAG expression in mature B lymphocytes. To assess the significance of this mechanism for the pathogenesis of malignant lymphomas, we have examined the expression of RAG genes in 11 cases of EBV‐associated endemic Burkitt's lymphoma (BL), 25 cases of Hodgkin's disease (HD, 17 EBV + , 8 EBV ‐ ) and 10 cases of follicular non‐Hodgkin's lymphoma (NHL). Using in situ hybridization, expression of the RAGs was detected in cortical thymocytes in normal thymus and in the tumor cells of 2 of 3 lymphoblastic NHL. By contrast, there was no detectable RAG expression in the BL, HD and follicular NHL cases. Our results indicate that re‐induction of RAG expression does not occur in human lymphomas in vivo . Thus, it is unlikely to play a role in the development of translocations involving immunoglobulin gene loci which are characteristically found in BL and follicular NHL. Moreover, our study shows that in situ hybridization is a suitable method for the analysis of RAG expression in human tissue sections. © 2001 Wiley‐Liss, Inc.