Evidence map›Paper›PMID 22275381›Full record

ReviewBlood2012

Dysfunction of the TP53 tumor suppressor gene in lymphoid malignancies.

Zijun Y Xu-Monette, L Jeffrey Medeiros, Yong Li, Robert Z Orlowski, Michael Andreeff, Carlos E Bueso-Ramos, Timothy C Greiner, Timothy J McDonnell, Ken H Young

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Molecular origin, discovery, validation and application of neoantigens.Asian journal of pharmaceutical sciences · 2026
    Review
  3. Article
  4. Article
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  7. iScience · 2025
    Article
  8. Article
  9. Review
  10. Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 2025
    Review
  11. Article
  12. Review
  13. Review
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  16. Review
  17. Article
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  20. Article

36 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

9 authors at 4 institutions in 1 country.

Zijun Y Xu-MonetteDepartment of Hematopathology, University of Texas MD Anderson Cancer Center, Houston, USA.
L Jeffrey Medeiros
Yong Li
Robert Z Orlowski
Michael Andreeff
Carlos E Bueso-Ramos
Timothy C Greiner
Timothy J McDonnell
Ken H Young
The University of Texas MD Anderson Cancer Center · USLymphoma Research Foundation · USUniversity of Louisville · USUniversity of Nebraska Medical Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
P4 -TARGETING MULTIPLE MYELOMA BY COMBINING CDK INHIBITORS AND BCL-2 ANTAGONISTSP50CA142509 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KWAK, LARRY W · 2010 to 2014
$11.1M
Convergence of MicroRNAs and p53 Signaling in Multiple Myeloma: Environmental CoR01CA138688 · NCI · UNIVERSITY OF LOUISVILLE · PI LI, YONG · 2009 to 2017
$2.9M
Deep Sequencing of Small Regulatory RNAs in Diffuse Large B cell LymphomaRC1CA146299 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI XIAO, CHANGCHUN · 2009 to 2010
$1000k
NCI NIH HHS 1RC1CA146299NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA142509NCI NIH HHS P50CA142509NCI NIH HHS R01 CA138688NCI NIH HHS R01CA138688NCI NIH HHS RC1 CA146299
6 · The paper itself

Abstract

Mutations of the TP53 gene and dysregulation of the TP53 pathway are important in the pathogenesis of many human cancers, including lymphomas. Tumor suppression by p53 occurs via both transcription-dependent activities in the nucleus by which p53 regulates transcription of genes involved in cell cycle, DNA repair, apoptosis, signaling, transcription, and metabolism; and transcription-independent activities that induces apoptosis and autophagy in the cytoplasm. In lymphoid malignancies, the frequency of TP53 deletions and mutations is lower than in other types of cancer. Nonetheless, the status of TP53 is an independent prognostic factor in most lymphoma types. Dysfunction of TP53 with wild-type coding sequence can result from deregulated gene expression, stability, and activity of p53. To overcome TP53 pathway inactivation, therapeutic delivery of wild-type p53, activation of mutant p53, inhibition of MDM2-mediated degradation of p53, and activation of p53-dependent and -independent apoptotic pathways have been explored experimentally and in clinical trials. We review the mechanisms of TP53 dysfunction, recent advances implicated in lymphomagenesis, and therapeutic approaches to overcoming p53 inactivation.

Indexed as

HumansLymphocytesLymphomaMicroRNAsSignal TransductionTranscription, GeneticTumor Suppressor Protein p53MicroRNAsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22275381
PMCPMC3335376
OpenAlexW2087945287

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.