Evidence map›Paper›PMID 19302140›Full record

ReviewImmunology2009

Restricting activation-induced cytidine deaminase tumorigenic activity in B lymphocytes.

Rafael Casellas, Arito Yamane, Alexander L Kovalchuk, Michael Potter

Open access · greenAbstract readReview
In one paragraph

Review in Immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  5. Enhancer biology and enhanceropathies.Nature structural & molecular biology · 2014
    Review
  6. Article
  7. Article
  8. Review
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  10. Mouse model of endemic Burkitt translocations reveals the long-range boundaries of Ig-mediated oncogene deregulation.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  11. Article
  12. Article
  13. Article
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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

4 authors at 1 institution in 1 country.

Rafael CasellasGenomics and Immunity, NIAMS, National Institutes of Health, Bethesda, MD 20892, USA. casellar@mail.nih.gov
Arito Yamane
Alexander L Kovalchuk
Michael Potter
National Institutes of Health · US

Funding

RAG and AID biologyZIAAR041148 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2025
$44.8M
NIAMS Light Imaging FacilityZICAR041186 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RANDAZZO, DAVIDE · 2010 to 2025
$18.2M
Transcription, Chromatin and DNA repairZIAAR041149 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI CASELLAS, RAFAEL C · 2009 to 2010
$2.2M
Transcription, Chromatin and DNA RepairZ01AR041149 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI CASELLAS, RAFAEL C · 2005 to 2008
$1.8M
AID biologyZ01AR041148 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI CASELLAS, RAFAEL C · 2005 to 2008
$1.8M
PATHOGENESIS OF PLASMA CELL TUMORS IN MICEZ01BC005596 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POTTER, MICHAEL · 1996 to 2008
$1.7M
Pathogenesis of plasma cell tumors in miceZIABC005596 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POTTER, MICHAEL · 2009 to 2009
$388k
Intramural NIH HHS
6 · The paper itself

Abstract

DNA breaks play an essential role in germinal centre B cells as intermediates to immunoglobulin class switching, a recombination process initiated by activation-induced cytidine deaminase (AID). Immunoglobulin gene hypermutation is likewise catalysed by AID but is believed to occur via single-strand DNA breaks. When improperly repaired, AID-mediated lesions can promote chromosomal translocations (CTs) that juxtapose the immunoglobulin loci to heterologous genomic sites, including oncogenes. Two of the most studied translocations are the t(8;14) and T(12;15), which deregulate cMyc in human Burkitt's lymphomas and mouse plasmacytomas, respectively. While a complete understanding of the aetiology of such translocations is lacking, recent studies using diverse mouse models have shed light on two important issues: (1) the extent to which non-specific or AID-mediated DNA lesions promote CTs, and (2) the safeguard mechanisms that B cells employ to prevent AID tumorigenic activity. Here we review these advances and discuss the usage of pristane-induced mouse plasmacytomas as a tool to investigate the origin of Igh-cMyc translocations and B-cell tumorigenesis.

Indexed as

AnimalsB-LymphocytesCell Transformation, NeoplasticCytidine DeaminaseGenes, Immunoglobulin Heavy ChainGenes, mycLymphocyte ActivationMicePlasmacytomaSomatic Hypermutation, ImmunoglobulinTranslocation, GeneticCytidine Deaminase

Identifiers

PMID19302140
PMCPMC2669812
OpenAlexW2026304664

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.