Evidence map›Paper›PMID 40562832›Full record

ArticleCell death and differentiation2025

p53 prophylactic therapy for cancer prevention.

Christian Krueger, Kanaga Sabapathy

Abstract read
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. Review
  2. Unveiling the Pharmacological Potential ofInternational journal of molecular sciences · 2026
    Article
  3. Article
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.

Christian KruegerDivision of Cellular & Molecular Research, National Cancer Centre Singapore, Singapore, Singapore.
Kanaga SabapathyDivision of Cellular & Molecular Research, National Cancer Centre Singapore, Singapore, Singapore. kanaga.sabapathy@ntu.edu.sg.ORCID 0000-0002-4346-7386

Funding

MOH | National Medical Research Council (NMRC) NA
6 · The paper itself

Abstract

Germline mutations in the tumor suppressor TP53 lead to cancer predisposition, as seen in Li-Fraumeni syndrome (LFS). Currently, no strategies exist to delay or prevent cancer development in this population. Our work is based on the hypothesis that modulating wild-type p53 levels could serve as a prophylactic approach to mitigate cancer risk. By introducing a third copy of Trp53, either constitutively or in an inducible manner in adulthood, we demonstrate that tumor development is delayed, and mice live longer without observable side effects in both the Eu-myc lymphoma and LFS models. Mechanistically, Trp53 loss of heterozygosity is reduced in the LFS model, accompanied by an enhanced p53 transcriptional response. Our findings therefore provide genetic evidence supporting this approach, which could be leveraged to identify compounds that modulate p53 levels and benefit LFS carriers and other cancer-prone populations with reduced p53 activity.

Indexed as

Li-Fraumeni SyndromeNeoplasmsTumor Suppressor Protein p53AnimalsHumansLoss of HeterozygosityMiceTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID40562832
PMCPMC12669783

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.