Evidence map›Paper›PMID 21123835›Full record

ArticleCarcinogenesis2011

The role of TP53 and MDM2 polymorphisms in TP53 mutagenesis and risk of non-melanoma skin cancer.

Lindsay M Almquist, Margaret R Karagas, Brock C Christensen, Marleen M Welsh, Ann E Perry, Craig A Storm, Heather H Nelson

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 3 pooled it
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 3 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Genetic association between p53 codon 72 polymorphism and risk of cutaneous squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Influence ofOncoTargets and therapy · 2016
    Article
  11. p53 Arg72Pro polymorphism and risk of basal cell carcinoma: a meta analysis.International journal of clinical and experimental medicine · 2015
    Article
  12. Review
  13. Article
  14. Review
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

7 authors at 5 institutions in 1 country.

Lindsay M AlmquistDivision of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN 55455, USA.
Margaret R Karagas
Brock C Christensen
Marleen M Welsh
Ann E Perry
Craig A Storm
Heather H Nelson
Dartmouth–Hitchcock Medical Center · USUniversity of Minnesota Medical Center · USCenter for Environmental Health · USCotton (United States) · USUniformed Services University of the Health Sciences · US

Funding

NONMELANOMA SKIN CANCER IN NEW HAMPSHIRER01CA057494 · NCI · DARTMOUTH COLLEGE · PI KARAGAS, MARGARET RITA · 1993 to 2015
$10.9M
MOLECULAR EPIDEMIOLOGY OF NON-MELANOMA SKIN CANCERR01CA082354 · NCI · UNIVERSITY OF MINNESOTA · PI NELSON, HEATHER HAMMOND · 1999 to 2011
$4.2M
NCI NIH HHS CA057494NCI NIH HHS CA082354NCI NIH HHS R01 CA057494NCI NIH HHS R01 CA082354
6 · The paper itself

Abstract

P53 is a key regulatory molecule in the cellular response to ultraviolet radiation, and TP53 mutation is the most common alteration in non-melanoma skin cancer. The MDM2 oncogene negatively regulates p53 protein levels, and both genes have functional polymorphisms that may modify skin cancer risk. Furthermore, prior research suggests that TP53 mutations preferentially occur on the arginine allele to selectively inactivate the p63 pathway. We tested these hypotheses of susceptibility and preferential mutation in non-melanoma skin cancer. The TP53 Arg72Pro and MDM2 309 polymorphisms were genotyped in a population-based case-control study of non-melanoma skin cancer, and TP53 alteration (mutation and immunohistochemistry staining) was evaluated in case tumors. In 902 cases of basal cell carcinoma (BCC), 676 cases of squamous cell carcinoma (SCC) and 812 controls, no association was found between the TP53 polymorphism and risk of non-melanoma skin cancer [odds ratio (OR)(BCC) 0.98, 95% confidence interval (CI) 0.80-1.20; OR(SCC) 0.93, 95% CI 0.75-1.16]. However, carriers of the MDM2 SNP309 G allele did have an elevated risk of non-melanoma skin cancer (OR(BCC) 1.15, 95% CI 0.93-1.42; OR(SCC) 1.29, 95% CI 1.02-1.63). We observed an association between TP53 alterations in the tumors and constitutive TP53 genotype (P < 0.01), with alterations preferentially occurring on the proline allele. Collectively, these data highlight the significant effects of genotype on gene-specific mutation events in carcinogenesis.

Indexed as

AdultAgedBasal Cell CarcinomaCarcinoma, Squamous CellCase-Control StudiesDNA, NeoplasmFemaleGenetic Predisposition to DiseaseGenotypeHumansImmunoenzyme TechniquesMaleMiddle AgedMutationPolymerase Chain ReactionPolymorphism, Single NucleotideDNA, NeoplasmMDM2 protein, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID21123835
PMCPMC3105583
OpenAlexW2130480587

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.