Evidence map›Paper›PMID 15077144›Full record

ReviewOncogene2004

To die or not to die: how does p53 decide?

Elizabeth A Slee, Daniel J O'Connor, Xin Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing 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

76 citing papers in PubMed.

  1. Article
  2. Biomarkers and intermediate-high risk non-muscle invasive bladder cancer: a multivariate analysis of three different cellular pathways with pronostic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Observational
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  18. Article
  19. Article
  20. Review

16 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.

Elizabeth A SleeImperial College School of Medicine at St Mary's, Ludwig Institute for Cancer Research, Norfolk Place, London W2 1PG, UK.
Daniel J O'Connor
Xin Lu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is frequently mutated in cancer and as a result is one of the most intensely studied tumour suppressors. Analysis of the primitive forms of p53 found in Caenorhabditis elegans and Drosophila, alongside studies using transgenic mouse models, indicate that the induction of apoptosis is both the most conserved function of p53 and vital for tumour suppression. p53-mediated apoptosis occurs through a combination of mechanisms which include pathways that are both dependent and independent of alterations in gene expression. In response to genotoxic insult, these pathways probably act together, thereby amplifying the apoptotic signal. However, the picture is complicated because the p53 activity is determined by stress type and individual cellular characteristics. The numerous p53 responsive genes that have been identified also provide further means of controlling the actions of p53. The recent discoveries of proteins that interact with p53 and specifically regulate the ability of p53 to trigger apoptosis have provided further mechanistic insights into the role of p53 in inducing cell death. Understanding the molecular basis of the proapoptotic action of p53 can assist in our quest to reintroduce or reactivate p53 in human tumours.

Indexed as

ApoptosisAnimalsGenes, p53HumansMutationNeoplasmsOrgan SpecificityTranscription, GeneticTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID15077144

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.