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• W2023301036 abstract "Epstein–Barr virus (EBV) can infect T lymphocytes and manifests as hemophagocytic lymphohistiocytosis (HLH), a distinct entity of hemophagocytic syndrome (HPS) characterized by fever, hepatosplenomegaly, cytopenia, hypercytokinemia, and systemic macrophage activation with hemophagocytosis. In a substantial percentage of HLH patients, the disease may relapse or progress to T-cell lymphoma in months to years. In the present review, the authors summarize the previous studies on the pathogenesis of HLH and the potential mechanism for the progression of disease from HLH to T-cell lymphoma. The infection of T cells by EBV could activate T cells to secrete proinflammatory cytokines, particularly tumor necrosis factor-α (TNF-α), which subsequently activate macrophages. EBV latent membrane protein-1 (LMP-1) is the viral product responsible for the activation of the TNF receptor (TNFR) associated factors/nuclear factor-κB (NF-κB)/ERK pathway to enhance cytokine secretion mediated through the suppression of the SAP/SH2D1A gene. The activation of NF-κB will confer resistance to TNF-α-induced apoptosis on EBV-infected T cells through the down-regulation of TNFR-1. Consistent with in vitro observations, EBV-associated T or natural killer/T-cell lymphoma showed constitutive activation of NF-κB, explaining its drug resistance, hypercytokinemia, and poor prognosis. Therefore, similar to other inflammation-associated cancers, HLH provides a unique model to study the mechanism of disease progression from a benign virus-infected disorder (HLH) to T-cell lymphoma. Inhibition of the NF-κB signal pathway should provide a potential target for the treatment of HLH and EBV-associated T-cell lymphoma. (Cancer Sci 2007; 98: 1281–1287)" @default.
• W2023301036 created "2016-06-24" @default.
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• W2023301036 date "2007-09-01" @default.
• W2023301036 modified "2023-10-12" @default.
• W2023301036 title "Pathogenesis and mechanism of disease progression from hemophagocytic lymphohistiocytosis to Epstein-Barr virus-associated T-cell lymphoma: Nuclear factor-κB pathway as a potential therapeutic target" @default.
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• W2023301036 doi "https://doi.org/10.1111/j.1349-7006.2007.00549.x" @default.
• W2023301036 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17627615" @default.
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