Evidence map›Paper›PMID 20371343›Full record

ReviewCell2010

Origin of chromosomal translocations in lymphoid cancer.

André Nussenzweig, Michel C Nussenzweig

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 2 pooled it
14.3field-weighted citation impact, top 1% 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

183 citing papers in PubMed, 2 syntheses or guidelines pooled it, 303 citations in OpenAlex.

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  9. Biomolecular condensates in immune cell fate.Nature reviews. Immunology · 2025
    Review
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123 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

2 authors at 2 institutions in 1 country.

André NussenzweigExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. andre_nussenzweig@nih.gov
Michel C Nussenzweig
Howard Hughes Medical Institute · USNational Institutes of Health · US

Funding

DNA RepairZIABC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Relationship between DNA damage detection and signalingZIABC010959 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
Class Switch Recombination in B LymphocytesR37AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 2014 to 2023
$5.4M
SIGNALLING PATHWAYS IN AUTOIMMUNITYR01AI037526 · NIAID · ROCKEFELLER UNIVERSITY · PI NUSSENZWEIG, MICHEL C · 1994 to 2012
$5.0M
DNA REPAIRZ01BC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 1998 to 2008
$2.9M
Relationship between DNA damage detection and signalingZ01BC010959 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2008 to 2008
$812k
Howard Hughes Medical InstituteIntramural NIH HHS Z01 BC010283Intramural NIH HHS Z01 BC010959Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC010283NIAID NIH HHS AI037526NIAID NIH HHS R01 AI037526NIAID NIH HHS R37 AI037526
6 · The paper itself

Abstract

Aberrant fusions between heterologous chromosomes are among the most prevalent cytogenetic abnormalities found in cancer cells. Oncogenic chromosomal translocations provide cells with a proliferative or survival advantage. They may either initiate transformation or be acquired secondarily as a result of genomic instability. Here, we highlight recent advances toward understanding the origin of chromosomal translocations in incipient lymphoid cancers and how tumor-suppressive pathways normally limit the frequency of these aberrant recombination events. Deciphering the mechanisms that mediate chromosomal fusions will open new avenues for developing therapeutic strategies aimed at eliminating lesions that lead to the initiation, maintenance, and progression of cancer.

Indexed as

Translocation, GeneticHumansLymphomaTumor Suppressor ProteinsTumor Suppressor Proteins

Identifiers

PMID20371343
PMCPMC2874895
OpenAlexW2117973542

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.