Frequent expression of the tumor necrosis factor receptor–associated factor 1 in latent membrane protein 1–Positive posttransplant lymphoproliferative disease and HIV-associated lymphomas
The tumor necrosis factor receptor–associated factor 1 (TRAF1) participates in the signal transduction of various members of the tumor necrosis factor receptor (TNFR) family, including TNFR2, CD40, CD30, and the Epstein-Barr virus (EBV)–encoded latent membrane protein 1 (LMP1). In vitro, TRAF1 is in...
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Published in | Human pathology Vol. 32; no. 9; pp. 963 - 969 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.09.2001
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | The tumor necrosis factor receptor–associated factor 1 (TRAF1) participates in the signal transduction of various members of the tumor necrosis factor receptor (TNFR) family, including TNFR2, CD40, CD30, and the Epstein-Barr virus (EBV)–encoded latent membrane protein 1 (LMP1). In vitro, TRAF1 is induced by LMP1, and previous studies have suggested that expression of TRAF1 is higher in EBV-associated tumors than in their EBV-negative counterparts. To determine whether this was the case in posttransplant lymphoproliferative disease (PTLD) and related disorders, we used immunohistochemistry to analyze expression of TRAF1 in a total of 42 such lesions arising in a variety of immunosuppressive states. The specimens consisted of 22 PTLD lesions, 18 acquired immunodeficiency syndrome–associated lymphomas, including 6 primary central nervous system lymphomas, and 2 cases of Hodgkin disease. The presence of latent EBV infection was determined by EBER in situ hybridization, and expression of EBV-LMP1 was detected by immunohistochemistry. Latent EBV infection, as determined by a positive EBER signal, was detected in 36 of 42 tumors. Of the EBER-positive specimens, 30 of 36 also expressed LMP1. Twenty-four of 30 LMP1-positive tumors, including both Hodgkin disease specimens, expressed TRAF1, compared with only 3 of 12 LMP1-negative tumors. This difference was statistically significant (P <.005). These results show frequent expression of TRAF1 at the protein level in LMP1-positive PTLD and related disorders and suggest an important role for LMP1-mediated TRAF1 signaling in the pathogenesis of EBV-positive tumors arising in immunosuppressive states. HUM PATHOL 32:963-969. Copyright © 2001 by W.B. Saunders Company |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0046-8177 1532-8392 |
DOI: | 10.1053/hupa.2001.27114 |