Evidence map›Paper›PMID 33323382›Full record

ArticleCancer research2021

Robust p53 Stabilization Is Dispensable for Its Activation and Tumor Suppressor Function.

Ning Kon, Michael Churchill, Huan Li, Siddhartha Mukherjee, James J Manfredi, Wei Gu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. LFPM inhibition of RING1-mediated p53Cell death and differentiation · 2026
    Article
  2. Unraveling the role ofHemaSphere · 2026
    Review
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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

6 authors at 3 institutions in 1 country.

Ning KonInstitute for Cancer Genetics, Department of Pathology and Cell Biology, and Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons, Columbia University, New York, New York.
Michael ChurchillDepartment of Medicine and Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons, Columbia University, New York, New York.ORCID https://orcid.org/0000-0001-7202-3891
Huan LiInstitute for Cancer Genetics, Department of Pathology and Cell Biology, and Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons, Columbia University, New York, New York.
Siddhartha MukherjeeDepartment of Medicine and Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons, Columbia University, New York, New York.
James J ManfrediDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
Wei GuInstitute for Cancer Genetics, Department of Pathology and Cell Biology, and Herbert Irving Comprehensive Cancer Center, College of Physicians & Surgeons, Columbia University, New York, New York. wg8@cumc.columbia.edu.
Cancer Genetics (United States) · USColumbia University · USIcahn School of Medicine at Mount Sinai · US

Funding

Regulation of p53 acetylation and deacetylation in tumorigenesis.R01CA085533 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2000 to 2021
$5.2M
Novel small molecule USP7 Inhibitors for p53 activation and cancer therapyR01CA254970 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2021 to 2025
$1.8M
Regulation of SLC7A11 by p53 in cancer metabolismR01CA190477 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2016 to 2020
$1.8M
Mechanisms of targeting oncoprotein SET in tumor suppressionR01CA216884 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2017 to 2021
$1.8M
p53 acetylation in ferroptosis and tumor suppressionR01CA224272 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GU, WEI · 2018 to 2021
$1.5M
NCI NIH HHS R01 CA085533NCI NIH HHS R01 CA190477NCI NIH HHS R01 CA216884NCI NIH HHS R01 CA224272NCI NIH HHS R01 CA254970
6 · The paper itself

Abstract

p53 is a short-lived protein with low basal levels under normal homeostasis conditions. However, upon DNA damage, levels of p53 dramatically increase for its activation. Although robust stabilization of p53 serves as a "trademark" for DNA damage responses, the requirement for such dramatic protein stabilization in tumor suppression has not been well addressed. Here we generated a mutant

Indexed as

AcetylationAnimalsApoptosisCarcinoma, Pancreatic DuctalCells, CulturedDNA DamageGenes, Tumor SuppressorLysineMiceMice, TransgenicMutant ProteinsMutationPancreatic NeoplasmsProtein Processing, Post-TranslationalProtein StabilityTranscriptional ActivationLysineMutant ProteinsTumor Suppressor Protein p53

Identifiers

PMID33323382
PMCPMC8026563
OpenAlexW3112267542

What OpenQuestion holds

Textmetadata
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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.