Evidence map›Paper›PMID 24942866›Full record

ReviewCarcinogenesis2014

Caught in the cross fire: p53 in inflammation.

Tomer Cooks, Curtis C Harris, Moshe Oren

Open access · bronzeAbstract readReview
In one paragraph

Review in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Frontiers in oncology · 2025
    Review
  9. iScience · 2024
    Article
  10. Article
  11. Article
  12. Mutant p53Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  13. DDX20: A Multifunctional Complex Protein.Molecules (Basel, Switzerland) · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

31 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

3 authors at 1 institution in 1 country.

Tomer CooksLaboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD 20892-4258, USA and Molecular Cell Biology, Weizmann Institute for Science, Rehovot 76100, Israel tomer.cooks@nih.gov.
Curtis C HarrisLaboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD 20892-4258, USA and Molecular Cell Biology, Weizmann Institute for Science, Rehovot 76100, Israel.
Moshe OrenMolecular Cell Biology, Weizmann Institute for Science, Rehovot 76100, Israel.
Weizmann Institute of Science · IL

Funding

p53, Aging, and CancerZIABC011496 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2013 to 2025
$21.1M
Functional analysis of the p53 tumor suppressorR37CA040099 · NCI · WEIZMANN INSTITUTE OF SCIENCE · PI OREN, MOSHE · 2003 to 2012
$2.2M
Intramural NIH HHSNCI NIH HHS R37 CA40099
6 · The paper itself

Abstract

The p53 transcription factor is a major tumor suppressor, whose diverse activities serve to ensure genome stability and inhibit neoplastic processes. In recent years, it is becoming increasingly clear that p53 also plays a broader role in maintaining cellular homeostasis, as well as contributing to tissue homeostasis in a non-cell-autonomous fashion. Chronic inflammation is a potential cancer-promoting condition, and as such is also within the radar of p53, which mounts a multifaceted attempt to prevent the escalation of chronic tissue imbalance into neoplasia. Recent understanding of the p53 pathway and other family members reveals a broad interaction with inflammatory elements such as reactive oxygen and nitrogen species, cytokines, infectious agents and major immune-regulatory pathways like nuclear factor-kappaB. This complex cross talk is highly dependent on p53 status, as different p53 isoforms and p53 mutants can mediate different responses and even promote chronic inflammation and associated cancer, acting in the tumor cells as well as in the stromal and immune compartments.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsHumansInflammationNeoplasmsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID24942866
PMCPMC4123652
OpenAlexW2167572981

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.