Evidence map›Paper›PMID 19182823›Full record

ArticleOncogene2009

Epstein-Barr virus LMP2A accelerates MYC-induced lymphomagenesis.

R Bultema, R Longnecker, M Swanson-Mungerson

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Rewiring of B cell receptor signaling by Epstein-Barr virus LMP2A.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Mouse model of Epstein-Barr virus LMP1- and LMP2A-driven germinal center B-cell lymphoproliferative disease.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015
    Review
  16. Article
  17. Article
  18. EBV-related lymphomas: new approaches to treatment.Current treatment options in oncology · 2013
    Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

R BultemaDepartment of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
R Longnecker
M Swanson-Mungerson
Northwestern University · US

Funding

In Vivo Model of Epstein-Barr Virus LatencyR01CA073507 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1997 to 2018
$6.1M
EBV LATENT MEMBRANE PROTEIN 2R01CA062234 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1994 to 2007
$2.2M
Discovery of New Treatment Options for EBV-associated Lymphoma and PTLDR01CA133063 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 2008 to 2012
$1.9M
NCI NIH HHS CA62234NCI NIH HHS CA73507NCI NIH HHS R01 CA062234NCI NIH HHS R01 CA073507NCI NIH HHS R01 CA133063
6 · The paper itself

Abstract

Despite the identification of Epstein-Barr virus (EBV) in tumors of Burkitt's lymphoma (BL) over 40 years ago, the exact contribution of EBV to BL is undefined. EBV encodes for multiple proteins in latent B cells that affect B cell survival and activation. One such protein, latent membrane protein 2A (LMP2A), protects B cells from numerous pro-apoptotic stimuli. Therefore, we tested whether LMP2A protects B cells from apoptosis induced by aberrant c-MYC expression that precedes and dominates BL. We crossed LMP2A-transgenic mice (LMP2A-Tg), in which all B cells express LMP2A, to a transgenic mouse that expresses a BL translocation of myc (lambda-MYC-Tg mice). LMP2A promotes proliferation and protects B cells from MYC-induced apoptosis in lambda-MYC-Tg mice. LMP2A also accelerates the development of lymphoma in LMP2A/lambda-MYC-Tg mice. Finally, LMP2A increases the expression of Bcl-X(L) in both pre-tumor B cells and tumor cells, suggesting a mechanism for LMP2A-mediated B cell survival in the presence of MYC. These results support a hypothesis that EBV LMP2A promotes tumor development by protecting pre-tumor B cells that would normally apoptose after the c-myc translocation.

Indexed as

Genes, mycAnimalsApoptosisbcl-X ProteinB-LymphocytesLymphocyte ActivationLymphomaMiceMice, TransgenicViral Matrix ProteinsBcl2l1 protein, mousebcl-X ProteinEBV-associated membrane antigen, Epstein-Barr virusViral Matrix Proteins

Identifiers

PMID19182823
PMCPMC2843388
OpenAlexW2084669567

What OpenQuestion holds

Textmetadata
LicenceTDM
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.