Evidence map›Paper›PMID 21566457›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Tissue-specific apoptotic effects of the p53 codon 72 polymorphism in a mouse model.

Gregory A Azzam, Amanda K Frank, Monica Hollstein, Maureen E Murphy

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Targeting PSAT1 to mitigate metastasis in tumors with p53-72Pro variant.Signal transduction and targeted therapy · 2023
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. The Codon 72Molecular cancer research : MCR · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Genetic Modifiers of the p53 Pathway.Cold Spring Harbor perspectives in medicine · 2016
    Review
  18. Article
  19. Effects of prostaglandin E2 on p53 mRNA transcription and p53 mutagenesis during T-cell-independent human B-cell clonal expansion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Gregory A AzzamFox Chase Cancer Center; Philadelphia PA, USA.
Amanda K Frank
Monica Hollstein
Maureen E Murphy
Fox Chase Cancer Center · USUniversity of Leeds · GB

Funding

Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
NCI NIH HHS R01 CA102184
6 · The paper itself

Abstract

Currently there are several dozen human polymorphisms that have been loosely associated with cancer risk. Correlating such variants with cancer risk has been challenging, primarily due to factors such as genetic heterogeneity, contributions of diet and environmental factors, and the difficulty in obtaining large sample sizes for analysis. Such difficulties can be circumvented with the establishment of mouse models for human variants. Recently, several groups have modeled human cancer susceptibility polymorphisms in the mouse. Remarkably, in each case these mouse models have accurately reflected human phenotypes, and clarified the contribution of these variants to cancer risk. We recently reported on a mouse model for the codon 72 polymorphism in p53, and found that this polymorphism regulates the ability to cooperate with NF-kB and induce apoptosis. Here-in we present evidence that this polymorphism impacts the apoptotic function of p53 in a tissue-specific manner; such tissue-specific effects of polymorphic variants represent an added challenge to human cancer risk association studies. The data presented here support the premise that modeling human polymorphisms in the mouse represents a powerful tool to assess the impact of these variants on cancer risk, progression and therapy.

Indexed as

Disease Models, AnimalAnimalsApoptosisCodonGene Knock-In TechniquesGenome-Wide Association StudyHumansMiceMice, Mutant StrainsNeoplasmsPolymorphism, GeneticRisk FactorsTissue DistributionTumor Suppressor Protein p53CodonTumor Suppressor Protein p53

Identifiers

PMID21566457
PMCPMC3117039
OpenAlexW2080382868

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.