Evidence map›Paper›PMID 24739573›Full record

ArticleNature reviews. Cancer2014

Unravelling mechanisms of p53-mediated tumour suppression.

Kathryn T Bieging, Stephano Spano Mello, Laura D Attardi

Open access · greenAbstract read
In one paragraph

Article in Nature reviews. Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 804 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
804citing papers in PubMed, 2 pooled it
53.8field-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

804 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,356 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
  2. Review of ferroptosis in colorectal cancer: Friends or foes?World journal of gastroenterology · 2023
    Pooled it
  3. Trial
  4. Article
  5. Article
  6. DFT design of PORSC advances · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Activating p53Nature communications · 2026
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

744 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.

Kathryn T BiegingDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.
Stephano Spano MelloDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.
Laura D Attardi1] Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA. [2] Department of Genetics, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.
Stanford University · US

Funding

Mouse Models to Dissect p53 Tumor Suppressor FunctionR01CA140875 · NCI · STANFORD UNIVERSITY · PI ATTARDI, LAURA D · 2011 to 2015
$1.7M
Elucidating p53 transcriptional networks involved in pancreatic cancer suppressioR21CA169673 · NCI · STANFORD UNIVERSITY · PI ATTARDI, LAURA D · 2012 to 2013
$368k
NCI NIH HHS R01 CA140875NCI NIH HHS R21 CA169673
6 · The paper itself

Abstract

p53 is a crucial tumour suppressor that responds to diverse stress signals by orchestrating specific cellular responses, including transient cell cycle arrest, cellular senescence and apoptosis, which are all processes associated with tumour suppression. However, recent studies have challenged the relative importance of these canonical cellular responses for p53-mediated tumour suppression and have highlighted roles for p53 in modulating other cellular processes, including metabolism, stem cell maintenance, invasion and metastasis, as well as communication within the tumour microenvironment. In this Opinion article, we discuss the roles of classical p53 functions, as well as emerging p53-regulated processes, in tumour suppression.

Indexed as

Genes, Tumor SuppressorAnimalsApoptosisCell Cycle CheckpointsCellular SenescenceDNA DamageHumansMiceNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsSignal TransductionStem CellsTranscriptional ActivationTranscription, GeneticTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24739573
PMCPMC4049238
OpenAlexW1966841369

What OpenQuestion holds

Textmetadata
LicenceTDM
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.