Evidence map›Paper›PMID 16492765›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis.

Julio C Morales, Sonia Franco, Michael M Murphy, Craig H Bassing, Kevin D Mills, Melissa M Adams, Nicole C Walsh, John P Manis, George Z Rassidakis, Frederick W Alt and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 99 citations in OpenAlex.

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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

11 authors at 5 institutions in 1 country.

Julio C MoralesDepartment of Biochemistry and Molecular Biology, University of Texas Health Sciences Center, Houston, 77030, USA.
Sonia Franco
Michael M Murphy
Craig H Bassing
Kevin D Mills
Melissa M Adams
Nicole C Walsh
John P Manis
George Z Rassidakis
Frederick W Alt
Phillip B Carpenter
Howard Hughes Medical Institute · USThe University of Texas Health Science Center at Houston · USBoston Children's Hospital · USHarvard University · USThe University of Texas MD Anderson Cancer Center · US

Funding

The Role of BCL-6 in Berminal Center FormationP01CA092625 · NCI · DANA-FARBER CANCER INSTITUTE · PI SHIPP, MARGARET A · 2001 to 2011
$32.9M
The Molecular Function of D-cyclins in T-ALLP01CA109901 · NCI · DANA-FARBER CANCER INSTITUTE · PI YOUNG, RICHARD · 2004 to 2014
$19.6M
Role of 53BP1 during the DNA damage responseR01GM065812 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CARPENTER, PHILLIP B · 2002 to 2006
$1.3M
Role of 53BP1 During the DNA Damage ResponseR56GM065812 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI CARPENTER, PHILLIP B · 2007 to 2007
$273k
NCI NIH HHS CA109901NCI NIH HHS CA92625NCI NIH HHS P01 CA092625NCI NIH HHS P01 CA109901NIGMS NIH HHS GM65812NIGMS NIH HHS R01 GM065812NIGMS NIH HHS R56 GM065812
6 · The paper itself

Abstract

p53-binding protein 1 (53BP1) participates in the cellular response to DNA double-stranded breaks where it associates with various DNA repair/cell cycle factors including the H2AX histone variant. Mice deficient for 53BP1 (53BP1(-/-)) are sensitive to ionizing radiation and immunodeficient because of impaired Ig heavy chain class switch recombination. Here we show that, as compared with p53(-/-) mice, 53BP1(-/-)/p53(-/-) animals more rapidly develop tumors, including T cell lymphomas and, at lower frequency, B lineage lymphomas, sarcomas, and teratomas. In addition, T cells from animals deficient for both 53BP1 and p53 (53BP1(-/-)/p53(-/-)) display elevated levels of genomic instability relative to T cells deficient for either 53BP1 or p53 alone. In contrast to p53(-/-) T cell lymphomas, which routinely display aneuploidy but not translocations, 53BP1(-/-)/p53(-/-) thymic lymphomas fall into two distinct cytogenetic categories, with many harboring clonal translocations (40%) and the remainder showing aneuploidy (60%). We propose that 53BP1, in the context of p53 deficiency, suppresses T cell lymphomagenesis through its roles in both cell-cycle checkpoints and double-stranded break repair.

Indexed as

AnimalsCells, CulturedCell Transformation, NeoplasticChromosomal Proteins, Non-HistoneChromosomes, MammalianCytosolDNA-Binding ProteinsGenomic InstabilityIntracellular Signaling Peptides and ProteinsLymphomaMiceMice, KnockoutMutationPhosphoproteinsSurvival RateThymus NeoplasmsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsPhosphoproteinsTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53

Identifiers

PMID16492765
PMCPMC1413919
OpenAlexW2146917785

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.