Frequent expression of the tumor necrosis factor receptor–associated factor 1 in latent membrane protein 1–Positive posttransplant lymphoproliferative disease and HIV-associated lymphomas

Murray, Paul G.; Swinnen, Lode J.; Flavell, Joanne R.; Ragni, Margaret V.; Baumforth, Karl R. N.; Toomey, S.; Filipovich, Alexandra H.; Lowe, Derek; Schnell, Carrie; Johl, J.; Gulley, Margaret L.; Lw, Young; Ambinder, Richard F.

doi:10.1053/hupa.2001.27114

Cited by 12 publications

(5 citation statements)

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“…It has been long established that latent membrane protein-1 (LMP1) is essential for Epstein-Barr virus (EBV)-mediated lymphocyte transformation (44, 91, 92). LMP1 recruits TRAF proteins, including TRAF1 to mimic CD40 receptor signaling in EBV-infected B lymphocytes leading to the activation of NF-κB, MAPK, phosphatidylinositol 3-kinase (PI3-K), IRF7, and STAT pathways (93).…”

Section: Infectious Diseasesmentioning

confidence: 99%

“…There is high and consistent TRAF1 overexpression in EBV-induced lymphoproliferations and Hodgkin's disease (44, 94). In addition, many cases of post-transplant lympho-proliferative disease and related disorders are TRAF1 positive (92). Siegler et al showed that TRAF1 co-localizes with LMP1 in EBV-infected cells in tonsillar cells of infectious mononucleosis patients (95).…”

Section: Infectious Diseasesmentioning

confidence: 99%

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TRAF1 Signaling in Human Health and Disease

2018

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Tumor necrosis factor receptor (TNFR) associated factor 1 (TRAF1) is a signaling adaptor first identified as part of the TNFR2 signaling complex. TRAF1 plays a key role in pro-survival signaling downstream of TNFR superfamily members such as TNFR2, LMP1, 4-1BB, and CD40. Recent studies have uncovered another role for TRAF1, independent of its role in TNFR superfamily signaling, in negatively regulating Toll-like receptor and Nod-like receptor signaling, through sequestering the linear ubiquitin assembly complex, LUBAC. TRAF1 has diverse roles in human disease. TRAF1 is overexpressed in many B cell related cancers and single nucleotide polymorphisms (SNPs) in TRAF1 have been linked to non-Hodgkin's lymphoma. Genome wide association studies have identified an association between SNPs in the 5′ untranslated region of the TRAF1 gene with increased incidence and severity of rheumatoid arthritis and other rheumatic diseases. The loss of TRAF1 from chronically stimulated CD8 T cells results in desensitization of the 4-1BB signaling pathway, thereby contributing to T cell exhaustion during chronic infection. These apparently opposing roles of TRAF1 as both a positive and negative regulator of immune signaling have led to some confusion in the literature. Here we review the role of TRAF1 as a positive and negative regulator in different signaling pathways. Then we discuss the role of TRAF1 in human disease, attempting to reconcile seemingly contradictory roles based on current knowledge of TRAF1 signaling and biology. We also discuss avenues for future research to further clarify the impact of TRAF1 in human disease.

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Section: Infectious Diseasesmentioning

confidence: 99%

Section: Infectious Diseasesmentioning

confidence: 99%

TRAF1 Signaling in Human Health and Disease

2018

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“…Therefore, we (R.F.A., R.B.M., and J.AD.) tested for tumor-cell EBV using in situ hybridization for EBV RNA (EBER1), with positive and negative controls, and standard immunohistochemical assays for EBV protein (LMP1), as described elsewhere (27,28), in paraffin-embedded tissue sections from the 311 HL patients (79% of 395) for whom usable pathology specimens could be retrieved. Among the 269 patients with known EBV tumor status and interview data, and therefore eligible for inclusion in these analyses, 37 (14%) had EBV-positive tumors, including 11% of women ages <45 years and 23% of women ages z45 years; 11% of non-Hispanic whites and 25% of all others; and 10% of the nodular sclerosis histologic subtype cases and 43% of mixed cellularity cases.…”

Section: Methodsmentioning

confidence: 99%

Body Size, Physical Activity, and Risk of Hodgkin's Lymphoma in Women

Keegan

Glaser

Clarke

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Few studies have examined the associations of body size and physical activity with the development of Hodgkin's lymphoma (HL) in women. In data from a population-based case-control study in women ages 19 to 79 years, we assessed the relation of self-report height, weight, body mass index (BMI), and strenuous physical activity to HL risk in 312 cases with diagnostic re-review and 325 randomdigit dialed controls using logistic regression. Analyses were stratified by age group and tumor cell presence of EBV. After adjustment for social class measures, taller childhood and adult height were associated with higher HL risk. In women ages 19 to 44 years, HL risk was elevated for higher, but healthy, BMI values, whereas in women ages 45 to 79 years, associations with BMI were inverse. The odds of developing HL were lower with participation (versus nonparticipation) in strenuous physical activity in the past year [odds ratio (OR), 0.58; 95% confidence interval (95% CI), 0.39-0.87 in women 19-44 years; OR, 0.45; 95% CI, 0.19-1.06 in women 45-79 years] and throughout adult life, and with sports team membership (versus nonmembership) in high school and/or at ages 18 to 22 years. Results were similar in cases (n = 269) with and without tumor-cell EBV compared with controls, although the inverse association with physical activity was somewhat stronger for women with EBV-positive disease. These findings show that in women, body size and strenuous physical activity, both modifiable characteristics, are associated with HL risk in adult life possibly through immunologic, infectious, or genetic mechanisms. (Cancer Epidemiol Biomarkers Prev 2006;15(6):1095 -101)

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“…It is only found in some epithelia, dendritic cells and activated lymphocytes 20,21 . In contrast, TRAF1 expression is upregulated in a variety of hematopoietic malignancies, such as chronic lymphocytic leukemias (CLL) 20 , non-Hodgkin lymphomas (NHL) 22 , Reed-Sternberg cells of Hodgkin disease 14,15 , LMP-1 positive post-transplant lymphoproliferative disease and HIV-associated lymphoma 23 , strongly suggesting a possible role for TRAF1 in the etiology of these B cell malignancies.…”

Section: Traf1 In B Cell Leukemia and Lymphomamentioning

confidence: 99%

Targeting TRAFs for Therapeutic Intervention

Zapata

Lefebvre²,

Reed³

Advances in Experimental Medicine and Biology

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TNF-receptor associated factors (TRAFs) are the molecules that upon engagement of the TNF-receptor (TNFR) by a TNF-family ligand come first in contact with the activated TNFR, initially acting as docking molecules for kinases and other effector proteins that are recruited to the activated receptor. TRAFs later regulate the subcellular relocalization of the receptor-ligand complex and finally they modulate the extent of the response by controlling the degradation of key proteins in the pathway. In this chapter, we review the involvement of different TRAF family members in the etiology of a variety of pathologies and address the question of whether the use of TNFR-mimic-peptides or small molecule modulators targeting TRAFs might be suitable for therapeutic intervention, discussing the advantages and disadvantages of this strategy.

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Frequent expression of the tumor necrosis factor receptor–associated factor 1 in latent membrane protein 1–Positive posttransplant lymphoproliferative disease and HIV-associated lymphomas

Cited by 12 publications

References 50 publications

TRAF1 Signaling in Human Health and Disease

TRAF1 Signaling in Human Health and Disease

Body Size, Physical Activity, and Risk of Hodgkin's Lymphoma in Women

Targeting TRAFs for Therapeutic Intervention

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