Evidence map›Paper›PMID 37067911›Full record

ArticleCancer discovery2023

Dimeric p53 Mutant Elicits Unique Tumor-Suppressive Activities through an Altered Metabolic Program.

Jovanka Gencel-Augusto, Xiaoping Su, Yuan Qi, Elizabeth M Whitley, Vinod Pant, Shunbin Xiong, Vrutant Shah, Jerome Lin, Encarnacion Perez, Marta L Fiorotto and 6 more

Open access · greenAbstract readEditorialComment
In one paragraph

Article in Cancer discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. LFPM inhibition of RING1-mediated p53Cell death and differentiation · 2026
    Article
  2. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
    Review
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  12. The Ashkenazi-Centric G334R Variant ofMolecular and cellular biology · 2024
    Article
  13. Article
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  16. Article
  17. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 1 country.

Jovanka Gencel-AugustoThe University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, Texas.ORCID 0000-0003-1333-415X
Xiaoping SuDepartment of Bioinformatics and Computational Biology, MDACC, Houston, Texas.ORCID 0000-0003-1824-943X
Yuan QiDepartment of Bioinformatics and Computational Biology, MDACC, Houston, Texas.ORCID 0000-0001-9718-7593
Elizabeth M WhitleyDepartment of Veterinary Medicine and Surgery, MDACC, Houston, Texas.
Vinod PantDepartment of Genetics, The University of Texas MD Anderson Cancer Center (MDACC), Houston, Texas.ORCID 0000-0002-3286-1804
Shunbin XiongDepartment of Genetics, The University of Texas MD Anderson Cancer Center (MDACC), Houston, Texas.ORCID 0000-0003-3984-1774
Vrutant ShahDepartment of Genetics, The University of Texas MD Anderson Cancer Center (MDACC), Houston, Texas.ORCID 0000-0001-5342-6513
Jerome LinDepartment of Genetics, The University of Texas MD Anderson Cancer Center (MDACC), Houston, Texas.ORCID 0000-0002-5424-9499
Encarnacion PerezDepartment of Epigenetics and Molecular Carcinogenesis, MDACC, Houston, Texas.ORCID 0000-0002-4354-8653
Marta L FiorottoUnited States Department of Agriculture/Agricultural Research Service Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.ORCID 0000-0001-8475-4704
Iqbal MahmudDepartment of Bioinformatics and Computational Biology, MDACC, Houston, Texas.ORCID 0000-0001-7729-8122
Abhinav K JainDepartment of Epigenetics and Molecular Carcinogenesis, MDACC, Houston, Texas.ORCID 0000-0003-3268-514X
Philip L LorenziDepartment of Bioinformatics and Computational Biology, MDACC, Houston, Texas.ORCID 0000-0003-0385-7774
Nicholas E NavinThe University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, Texas.ORCID 0000-0002-2106-8624
Ellen R RichieThe University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, Texas.ORCID 0000-0003-0786-973X
Guillermina LozanoThe University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, Texas.ORCID 0000-0001-8985-4886
The University of Texas MD Anderson Cancer Center · USCore Laboratories (United States) · USGenesis Laboratories · USChildren's Nutrition Research Center at Baylor College of Medicine · USHouston Community College System · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
PATHWAY OF TUMOR SUPPRESSIONR01CA047296 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GUILLERMINA LOZANO · 1993 to 2026
$8.0M
Role of p53 Missense Mutations on Tumorigenesis in VivoR01CA082577 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 1999 to 2024
$7.3M
Orbitrap Elite High-Resolution Mass Spectrometer for Proteomics and MetabolomicsS10OD012304 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HAWKE, DAVID H · 2013 to 2013
$877k
Identifying the vulnerabilities in Mdm2 overexpressing cancer cellsR50CA251703 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PANT, VINOD · 2020 to 2024
$418k
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA047296NCI NIH HHS R01 CA082577NCI NIH HHS R50 CA251703NIH HHS S10 OD012304
6 · The paper itself

Abstract

Cancer-related alterations of the p53 tetramerization domain (TD) abrogate wild-type (WT) p53 function. They result in a protein that preferentially forms monomers or dimers, which are also normal p53 states under basal cellular conditions. However, their physiologic relevance is not well understood. We have established in vivo models for monomeric and dimeric p53, which model Li-Fraumeni syndrome patients with germline p53 TD alterations. p53 monomers are inactive forms of the protein. Unexpectedly, p53 dimers conferred some tumor suppression that is not mediated by canonical WT p53 activities. p53 dimers upregulate the PPAR pathway. These activities are associated with lower prevalence of thymic lymphomas and increased CD8+ T-cell differentiation. Lymphomas derived from dimeric p53 mice show cooperating alterations in the PPAR pathway, further implicating a role for these activities in tumor suppression. Our data reveal novel functions for p53 dimers and support the exploration of PPAR agonists as therapies. SIGNIFICANCE: New mouse models with TP53R342P (monomer) or TP53A347D (dimer) mutations mimic Li-Fraumeni syndrome. Although p53 monomers lack function, p53 dimers conferred noncanonical tumor-suppressive activities. We describe novel activities for p53 dimers facilitated by PPARs and propose these are "basal" p53 activities. See related commentary by Stieg et al., p. 1046. See related article by Choe et al., p. 1250. This article is highlighted in the In This Issue feature, p. 1027.

Indexed as

Li-Fraumeni SyndromeAnimalsCell DeathMicePeroxisome Proliferator-Activated ReceptorsTranscriptional ActivationTumor Suppressor Protein p53Peroxisome Proliferator-Activated ReceptorsTumor Suppressor Protein p53

Identifiers

PMID37067911
PMCPMC10164062
OpenAlexW4366083167

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.