Evidence map›Paper›PMID 16550160›Full record

ReviewOncogene2006

Polymorphisms in the p53 pathway.

E C Pietsch, O Humbey, M E Murphy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 5 pooled it
–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

101 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. 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
  2. Pooled it
  3. Pooled it
  4. Polymorphisms of TP53 codon 72 with prostate carcinoma risk: a meta-analysis.Medical oncology (Northwood, London, England) · 2010
    Pooled it
  5. Pooled it
  6. Article
  7. Association of P53 Codon 72 Polymorphism with Ovarian Cancer: An Institutional Study.Asian Pacific journal of cancer prevention : APJCP · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. A Missense Variant inInternational journal of molecular sciences · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Anti-tumor activities ofJournal of ginseng research · 2021
    Article
  16. Article
  17. Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020
    Article
  18. Bioscience reports · 2019
    Article
  19. Association of theJournal of Cancer · 2019
    Article
  20. Article

41 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.

E C PietschDivision of Medical Sciences, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.
O Humbey
M E Murphy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor gene continues to be distinguished as the most frequently mutated gene in human cancer; this gene can be found mutated in up to 50% of human tumors of diverse histological type. It is generally accepted that the ability of p53 to induce either growth arrest or programmed cell death in response to diverse stimuli underlies the powerful selection against this protein in the development of cancer. It is somewhat surprising, then, to find p53 and several target genes in this pathway containing polymorphisms that impair their function. The nature of these polymorphic variants, and the mechanism whereby they impair the function of the p53 pathway, are reviewed here-in. The impact of these polymorphisms on cancer risk and the efficacy of therapy are only now becoming unraveled. Of particular relevance in these efforts will be the generation of mouse models of polymorphic variants in p53 and its target genes. Equally important will be better-controlled human studies, where-in haplotypes for p53 (that is, combinations of different polymorphisms in the p53 gene) and for p53-target genes are taken into account, instead of analyses of single gene variants, which have largely predominated to date. Studies in both regards should shed light on an emerging area in cancer biology, the significance of inter-individual differences in genotype on cancer risk, prognosis, and the efficacy of cancer therapy.

Indexed as

Polymorphism, GeneticAnimalsDisease Models, AnimalGenotypeHumansMiceNeoplasmsPrognosisRisk FactorsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID16550160

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.