Evidence map›Paper›PMID 35361963›Full record

ReviewCell death and differentiation2022

Mutant p53: it's not all one and the same.

Margaret C Kennedy, Scott W Lowe

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 1 pooled it
18.6field-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

139 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Determinants of CBiomolecules · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Reactivation ofInternational journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Unveiling the developmental and tumor-suppressive roles of the p53 variant p53psi.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  14. Article
  15. Pro-ATO/Allicin Liposomes for Dual-Pathway Targeting of p53-Mutant Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

79 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

2 authors at 1 institution in 1 country.

Margaret C KennedyCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA.ORCID http://orcid.org/0000-0001-9106-1906
Scott W LoweCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, 10065, USA. lowes@mskcc.org.ORCID http://orcid.org/0000-0002-5284-9650
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Mutation of the TP53 tumor suppressor gene is the most common genetic alteration in cancer, and almost 1000 alleles have been identified in human tumors. While virtually all TP53 mutations are thought to compromise wild type p53 activity, the prevalence and recurrence of missense TP53 alleles has motivated countless research studies aimed at understanding the function of the resulting mutant p53 protein. The data from these studies support three distinct, but perhaps not necessarily mutually exclusive, mechanisms for how different p53 mutants impact cancer: first, they lose the ability to execute wild type p53 functions to varying degrees; second, they act as a dominant negative (DN) inhibitor of wild type p53 tumor-suppressive programs; and third, they may gain oncogenic functions that go beyond mere p53 inactivation. Of these possibilities, the gain of function (GOF) hypothesis is the most controversial, in part due to the dizzying array of biological functions that have been attributed to different mutant p53 proteins. Herein we discuss the current state of understanding of TP53 allele variation in cancer and recent reports that both support and challenge the p53 GOF model. In these studies and others, researchers are turning to more systematic approaches to profile TP53 mutations, which may ultimately determine once and for all how different TP53 mutations act as cancer drivers and whether tumors harboring distinct mutations are phenotypically unique. From a clinical perspective, such information could lead to new therapeutic approaches targeting the effects of different TP53 alleles and/or better sub-stratification of patients harboring TP53 mutant cancers.

Indexed as

NeoplasmsTumor Suppressor Protein p53AllelesCarcinogenesisHumansMutant ProteinsMutationMutant ProteinsTumor Suppressor Protein p53

Identifiers

PMID35361963
PMCPMC9090915
OpenAlexW4220746635

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.