ArticleCell reports. Medicine2024
Multi-modal analysis reveals tumor and immune features distinguishing EBV-positive and EBV-negative post-transplant lymphoproliferative disorders.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Epstein-Barr virus infection in children with liver transplantation.World journal of hepatology · 2026Review
- NKG2A+ NK cell cytotoxicity of Epstein-Barr virus infected B cells is mediated through the NKG2D and NKp30 activating receptors.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Characterizing tumor microenvironment heterogeneity in EBVFrontiers in immunology · 2026Article
- Predictive biomarkers and preventive strategies for PTLD: a turning point in viro-immunologic precision medicine?Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
- Pescadillo ribosomal biogenesis factor 1 and programmed death-ligand 1 in gastric and head and neck squamous cell carcinoma.World journal of gastroenterology · 2025Article
- Delving deeper into the pathogenesis and genomics of posttransplant diffuse large B-cell lymphoma.HemaSphere · 2025Review
Corrections and comments
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Authors and funding
29 authors.
Funding
Abstract
The oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLDs). PTLD can also arise in the absence of EBV, but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions, respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines. We create a reference resource of proteins distinguishing EBV(+) B lymphoma cells from EBV(-) B lymphoma including the immunomodulatory molecules CD300a and CD24, respectively. Moreover, we show that CD300a is essential for maximal survival of EBV(+) PTLD B lymphoma cells. Our comprehensive multi-modal analyses uncover the biological underpinnings of PTLD and offer opportunities for precision therapies.
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Registered trials
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