Evidence map›Paper›PMID 24174629›Full record

ArticleBlood2014

Epstein-Barr virus latent membrane protein 2A enhances MYC-driven cell cycle progression in a mouse model of B lymphoma.

Kamonwan Fish, Jia Chen, Richard Longnecker

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  7. 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
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  19. EBV germinates lymphoma from the germinal center in a battle with T and NK cells.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. 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
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kamonwan FishDepartment of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Jia Chen
Richard Longnecker
Northwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
In Vivo Model of Epstein-Barr Virus LatencyR01CA073507 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1997 to 2018
$6.1M
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
Training Program in Viral ReplicationT32AI060523 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LAIMINS, LAIMONIS A. · 2004 to 2013
$1.4M
NCI NIH HHS CA073507NCI NIH HHS CA133063NCI NIH HHS NCI CA060553NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA073507NCI NIH HHS R01 CA133063NIAID NIH HHS T32 AI060523NIAID NIH HHS T32AI060523-09
6 · The paper itself

Abstract

Elevated expression of MYC is a shared property of many human cancers. Epstein-Barr virus (EBV) has been associated with lymphoid malignancies, yet collaborative roles between MYC and EBV in lymphomagenesis are unclear. EBV latent membrane protein 2A (LMP2A) functions as a B-cell receptor (BCR) mimic known to provide survival signals to infected B cells. Co-expression of human MYC and LMP2A in mice (LMP2A/λ-MYC) accelerates B lymphoma onset compared with mice expressing human MYC alone (λ-MYC mice). Here we show a novel role of LMP2A in potentiating MYC to promote G1-S transition and hyperproliferation by downregulating cyclin-dependent kinase inhibitor p27(kip1) in a proteasome-dependent manner. Expressing a gain-of-function S10A mutant of p27(kip1) has minor effect on tumor latency. However, pretumor B cells from λ-MYC mice expressing homozygous S10A mutant show a significant decrease in the percentage of S-phase cells. Interestingly, LMP2A is able to counteract the antiproliferative effect of the S10A mutant to promote S-phase entry. Finally, we show that LMP2A expression correlates with higher levels of MYC expression and suppression of p27(kip1) before lymphoma onset. Our study demonstrates a novel function of EBV LMP2A in maximizing MYC expression, resulting in hyperproliferation and cellular transformation into cancer cells in vivo.

Indexed as

Gene Expression Regulation, NeoplasticActive Transport, Cell NucleusAnimalsApoptosisCell CycleCell ProliferationCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p27Disease Models, AnimalFlow CytometryHomozygoteHumansLymphomaLymphoma, B-CellMiceMice, Inbred C57BLCyclin-Dependent Kinase Inhibitor p27EBV-associated membrane antigen, Epstein-Barr virusProto-Oncogene Proteins c-mycViral Matrix Proteins

Identifiers

PMID24174629
PMCPMC3901066
OpenAlexW2022548171

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.