Evidence map›Paper›PMID 22406538›Full record

ArticleThe Journal of clinical investigation2012

EBNA3B-deficient EBV promotes B cell lymphomagenesis in humanized mice and is found in human tumors.

Robert E White, Patrick C Rämer, Kikkeri N Naresh, Sonja Meixlsperger, Laurie Pinaud, Cliona Rooney, Barbara Savoldo, Rita Coutinho, Csaba Bödör, John Gribben and 9 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
8.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

104 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
  2. EBV Genome Variations and Association With Diseases.Journal of medical virology · 2026
    Review
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  5. Article
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  8. Article
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  14. Aflatoxin B1 and Epstein-Barr virus-induced CCL22 expression stimulates B cell infection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Review
  16. Article
  17. Article
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  19. Review
  20. Review

44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 3 countries.

Robert E WhiteSection of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Patrick C Rämer
Kikkeri N Naresh
Sonja Meixlsperger
Laurie Pinaud
Cliona Rooney
Barbara Savoldo
Rita Coutinho
Csaba Bödör
John Gribben
Hazem A Ibrahim
Mark Bower
Jamie P Nourse
Maher K Gandhi
Jaap Middeldorp
Fathima Z Cader
Paul Murray
Christian Münz
Martin J Allday
Imperial College London · GBImperial College Healthcare NHS Trust · GBQIMR Berghofer Medical Research Institute · AUUniversity of Birmingham · GBAmsterdam University Medical Centers · NLChelsea and Westminster Hospital · GB

Funding

Tissue ResourceP50CA126752 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MALCOLM K. BRENNER, HELEN E HESLOP · 2007 to 2026
$51.4M
VECTOR PRODUCTIONP01CA094237 · NCI · BAYLOR COLLEGE OF MEDICINE · PI HESLOP, HELEN E, ROONEY, CLIONA M. · 2002 to 2017
$27.8M
DC/NK interactions in human secondary lymphoid organsR01CA108609 · NCI · UNIVERSITY OF ZURICH · PI MUNZ, CHRISTIAN · 2004 to 2012
$1.8M
NCI NIH HHS P01 CA094237NCI NIH HHS P50 CA126752NCI NIH HHS R01 CA108609NCI NIH HHS R01CA108609Wellcome TrustWellcome Trust 077489
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) persistently infects more than 90% of the human population and is etiologically linked to several B cell malignancies, including Burkitt lymphoma (BL), Hodgkin lymphoma (HL), and diffuse large B cell lymphoma (DLBCL). Despite its growth transforming properties, most immune-competent individuals control EBV infection throughout their lives. EBV encodes various oncogenes, and of the 6 latency-associated EBV-encoded nuclear antigens, only EBNA3B is completely dispensable for B cell transformation in vitro. Here, we report that infection with EBV lacking EBNA3B leads to aggressive, immune-evading monomorphic DLBCL-like tumors in NOD/SCID/γc-/- mice with reconstituted human immune system components. Infection with EBNA3B-knockout EBV (EBNA3BKO) induced expansion of EBV-specific T cells that failed to infiltrate the tumors. EBNA3BKO-infected B cells expanded more rapidly and secreted less T cell-chemoattractant CXCL10, reducing T cell recruitment in vitro and T cell-mediated killing in vivo. B cell lines from 2 EBV-positive human lymphomas encoding truncated EBNA3B exhibited gene expression profiles and phenotypic characteristics similar to those of tumor-derived lines from the humanized mice, including reduced CXCL10 secretion. Screening EBV-positive DLBCL, HL, and BL human samples identified additional EBNA3B mutations. Thus, EBNA3B is a virus-encoded tumor suppressor whose inactivation promotes immune evasion and virus-driven lymphomagenesis.

Indexed as

Genes, Tumor SuppressorGenes, ViralAnimalsCell Line, TransformedCell Transformation, ViralChemokine CXCL10ChimeraDNA Mutational AnalysisEpstein-Barr Virus InfectionsEpstein-Barr Virus Nuclear AntigensGene DeletionHematopoietic Stem Cell TransplantationHerpesvirus 4, HumanHumansInterferon-gammaLymphoma, B-CellChemokine CXCL10CXCL10 protein, humanEBNA-3B antigenEpstein-Barr Virus Nuclear AntigensInterferon-gammaTumor Suppressor Proteins

Identifiers

PMID22406538
PMCPMC3314448
OpenAlexW1993365997

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.