Evidence map›Paper›PMID 22855598›Full record

ArticleBlood2012

Genome-wide analysis reveals recurrent structural abnormalities of TP63 and other p53-related genes in peripheral T-cell lymphomas.

George Vasmatzis, Sarah H Johnson, Ryan A Knudson, Rhett P Ketterling, Esteban Braggio, Rafael Fonseca, David S Viswanatha, Mark E Law, N Sertac Kip, Nazan Ozsan and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
12.7field-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

118 citing papers in PubMed, 232 citations in OpenAlex.

  1. Trial
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  4. Non-Haematologica · 2026
    Article
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  14. Programmed Death Ligand 1 (PD-L1) Expression in Lymphomas: State of the Art.International journal of molecular sciences · 2024
    Review
  15. Article
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  17. Article
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58 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

23 authors at 5 institutions in 2 countries.

George VasmatzisCenter for Individualized Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Sarah H Johnson
Ryan A Knudson
Rhett P Ketterling
Esteban Braggio
Rafael Fonseca
David S Viswanatha
Mark E Law
N Sertac Kip
Nazan Ozsan
Stefan K Grebe
Lori A Frederick
Bruce W Eckloff
E Aubrey Thompson
Marshall E Kadin
Dragana Milosevic
Julie C Porcher
Yan W Asmann
David I Smith
Irina V Kovtun
Stephen M Ansell
Ahmet Dogan
Andrew L Feldman
Mayo Clinic in Arizona · USMayo Clinic · USEge University · TRMayo Clinic in Florida · USProvidence College · US

Funding

The Role of Monocytes in non-Hodgkin LymphomaP50CA097274 · NCI · UNIVERSITY OF IOWA · PI WEINER, GEORGE J. · 2002 to 2021
$45.7M
6 · The paper itself

Abstract

Peripheral T-cell lymphomas (PTCLs) are aggressive malignancies of mature T lymphocytes with 5-year overall survival rates of only ∼ 35%. Improvement in outcomes has been stymied by poor understanding of the genetics and molecular pathogenesis of PTCL, with a resulting paucity of molecular targets for therapy. We developed bioinformatic tools to identify chromosomal rearrangements using genome-wide, next-generation sequencing analysis of mate-pair DNA libraries and applied these tools to 16 PTCL patient tissue samples and 6 PTCL cell lines. Thirteen recurrent abnormalities were identified, of which 5 involved p53-related genes (TP53, TP63, CDKN2A, WWOX, and ANKRD11). Among these abnormalities were novel TP63 rearrangements encoding fusion proteins homologous to ΔNp63, a dominant-negative p63 isoform that inhibits the p53 pathway. TP63 rearrangements were seen in 11 (5.8%) of 190 PTCLs and were associated with inferior overall survival; they also were detected in 2 (1.2%) of 164 diffuse large B-cell lymphomas. As TP53 mutations are rare in PTCL compared with other malignancies, our findings suggest that a constellation of alternate genetic abnormalities may contribute to disruption of p53-associated tumor suppressor function in PTCL.

Indexed as

Gene RearrangementMutationCell Line, TumorCyclin-Dependent Kinase Inhibitor p16DNA Mutational AnalysisFemaleGenome-Wide Association StudyHumansLymphoma, Large B-Cell, DiffuseLymphoma, T-Cell, PeripheralMaleMutant ProteinsOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionOxidoreductasesRepressor ProteinsANKRD11 protein, humanCyclin-Dependent Kinase Inhibitor p16Mutant ProteinsOncogene Proteins, FusionOxidoreductasesRepressor ProteinsTP53 protein, humanTP63 protein, humanTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsWW Domain-Containing OxidoreductaseWWOX protein, human

Identifiers

PMID22855598
PMCPMC5070713
OpenAlexW2085012601

What OpenQuestion holds

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Registered trials

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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.