Evidence map›Paper›PMID 40263541›Full record

ArticleCell death and differentiation2025

Integrative multiomic approaches reveal ZMAT3 and p21 as conserved hubs in the p53 tumor suppression network.

Anthony M Boutelle, Aicha R Mabene, David Yao, Haiqing Xu, Mengxiong Wang, Yuning J Tang, Steven S Lopez, Sauradeep Sinha, Janos Demeter, Ran Cheng and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors.

Anthony M BoutelleDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Aicha R MabeneDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
David YaoDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Haiqing XuDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-9124-3192
Mengxiong WangDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Yuning J TangDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Steven S LopezDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0009-0008-0926-0016
Sauradeep SinhaDepartment of Bioengineering, Stanford University Schools of Engineering and Medicine, Stanford, CA, USA.
Janos DemeterBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-7301-8055
Ran ChengBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, USA.
Brooks A BenardDivision of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Edel M McCreaDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Liz J ValenteDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA.
Alexandros P DrainasBioMed X Institute (GmbH), Heidelberg, Germany.
Martin FischerComputational Biology Group, Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.ORCID 0000-0002-3429-1876
Ravindra MajetiDivision of Hematology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Dmitri A PetrovDepartment of Biology, Stanford University, Stanford, CA, USA.
Peter K JacksonBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-1742-2539
Fan YangDepartment of Bioengineering, Stanford University Schools of Engineering and Medicine, Stanford, CA, USA.
Monte M WinslowDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Michael C BassikDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Laura D AttardiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA, USA. attardi@stanford.edu.ORCID 0000-0003-1782-9045

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Integrative approaches to elucidate p53 transcriptional networks during carcinogenesisR35CA197591 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI · 2015 to 2026
$11.6M
Unraveling mechanisms of tumor suppression in lung cancerR01CA234349 · NCI · STANFORD UNIVERSITY · PI PETROV, DMITRI, WINSLOW, MONTE MEIER · 2019 to 2023
$2.4M
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) R01CA234349Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) R35CA197591Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) T32CA009302NCI NIH HHS R01 CA234349NCI NIH HHS R35 CA197591NCI NIH HHS T32 CA009302Tobacco-Related Disease Research Program (TRDRP) 28IP-0037Tobacco-Related Disease Research Program (TRDRP) T31DT1713
6 · The paper itself

Abstract

TP53, the most frequently mutated gene in human cancer, encodes a transcriptional activator that induces myriad downstream target genes. Despite the importance of p53 in tumor suppression, the specific p53 target genes important for tumor suppression remain unclear. Recent studies have identified the p53-inducible gene Zmat3 as a critical effector of tumor suppression, but many questions remain regarding its p53-dependence, activity across contexts, and mechanism of tumor suppression alone and in cooperation with other p53-inducible genes. To address these questions, we used Tuba-seq

Indexed as

Cyclin-Dependent Kinase Inhibitor p21Lung NeoplasmsTumor Suppressor Protein p53Adenocarcinoma of LungAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMiceCyclin-Dependent Kinase Inhibitor p21Tumor Suppressor Protein p53

Identifiers

PMID40263541
PMCPMC12572384

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.