Evidence map›Paper›PMID 26024390›Full record

ReviewCell death and differentiation2015

TP53: an oncogene in disguise.

T Soussi, K G Wiman

Open access · hybridAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 1 pooled it
11.9field-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

189 citing papers in PubMed, 1 synthesis or guideline pooled it, 291 citations in OpenAlex.

  1. Influence ofJCO precision oncology · 2024
    Pooled it
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  5. Assessing the significance of CCNE1 overexpression in triple negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  19. Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025
    Review
  20. Article

129 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.

T Soussi1] Department of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK) R8:04, Stockholm SE-171 76, Sweden [2] Sorbonne Universités, UPMC Univ Paris 06, Paris F-75005, France [3] INSERM, U1138, Centre de Recherche des Cordeliers, Paris, France [4] Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
K G WimanDepartment of Oncology-Pathology, Karolinska Institutet, Cancer Center Karolinska (CCK) R8:04, Stockholm SE-171 76, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The standard classification used to define the various cancer genes confines tumor protein p53 (TP53) to the role of a tumor suppressor gene. However, it is now an indisputable fact that many p53 mutants act as oncogenic proteins. This statement is based on multiple arguments including the mutation signature of the TP53 gene in human cancer, the various gains-of-function (GOFs) of the different p53 mutants and the heterogeneous phenotypes developed by knock-in mouse strains modeling several human TP53 mutations. In this review, we will shatter the classical and traditional image of tumor protein p53 (TP53) as a tumor suppressor gene by emphasizing its multiple oncogenic properties that make it a potential therapeutic target that should not be underestimated. Analysis of the data generated by the various cancer genome projects highlights the high frequency of TP53 mutations and reveals that several p53 hotspot mutants are the most common oncoprotein variants expressed in several types of tumors. The use of Muller's classical definition of mutations based on quantitative and qualitative consequences on the protein product, such as 'amorph', 'hypomorph', 'hypermorph' 'neomorph' or 'antimorph', allows a more meaningful assessment of the consequences of cancer gene modifications, their potential clinical significance, and clearly demonstrates that the TP53 gene is an atypical cancer gene.

Indexed as

AnimalsAza CompoundsBridged Bicyclo Compounds, HeterocyclicHumansMaleimidesMutationPhenotypeTumor Suppressor Protein p531-(propoxymethyl)maleimide2,2-bis(hydroxymethyl)-1-azabicyclo(2,2,2,)octan-3-oneAza CompoundsBridged Bicyclo Compounds, HeterocyclicMaleimidesTumor Suppressor Protein p53

Identifiers

PMID26024390
PMCPMC4495363
OpenAlexW613972939

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.