Evidence map›Paper›PMID 18802452›Full record

ReviewCancer gene therapy2009

Recent advances in p53 research: an interdisciplinary perspective.

M Olivier, A Petitjean, V Marcel, A Pétré, M Mounawar, A Plymoth, C C de Fromentel, P Hainaut

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer gene therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 6 pooled it
9.6field-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

75 citing papers in PubMed, 6 syntheses or guidelines pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Association between p53 codon 72 polymorphism and sarcoma risk among Caucasians.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Review
  10. Tumor treating fields induced senescence on glioblastoma.American journal of cancer research · 2023
    Article
  11. A role for bioinorganic chemistry in the reactivation of mutant p53 in cancer.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. p53 drives a transcriptional program that elicits a non-cell-autonomous response and alters cell state in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Review
  19. Article
  20. Article

15 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

8 authors at 2 institutions in 1 country.

M Olivier1Group of Molecular Carcinogenesis and Biomarkers, International Agency for Research on Cancer, World Health Organization, Lyon, France. molivier@iarc.fr
A Petitjean
V Marcel
A Pétré
M Mounawar
A Plymoth
C C de Fromentel
P Hainaut
Centre International de Recherche sur le Cancer · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TP53 gene is one of the most studied genes in human cancer. In recent years, considerable interest was focused on mutant p53, the abnormal protein product of TP53 somatic or germline alleles with missense mutations that often accumulate in cancer cells. There is now compelling experimental evidence that many mutations can exert mutant-specific, gain-of-function effects by perturbing the regulation of expression of multiple genes. This notion is supported by the observation that targeted mutant p53 expression enhances the formation of specific cancers in the mouse even in the absence of wild-type p53 expression. In addition, clinical studies are producing a wealth of functional pathway data demonstrating correlations between specific TP53 mutations and gene expression patterns identified by transcriptome studies. These correlations imply that alteration of p53 function is critical in shaping gene expression patterns in cancer. Finally, progress is being made in the development of new therapeutic approaches targeting p53 alterations. Key advances regarding the structural, biochemical and functional properties of normal and mutant p53 proteins, their abnormal regulation and distribution in human cancers, and their associations with clinical and pathological cancer characteristics are reviewed. New opportunities for translational research for improving cancer detection, prognosis, prevention and therapy based upon the integration of this knowledge are described.

Indexed as

Mutation, MissenseAllelesAnimalsBiomedical ResearchGene Expression Regulation, NeoplasticHumansMiceNeoplasmsTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID18802452
OpenAlexW2018614123

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.