Evidence map›Paper›PMID 18701437›Full record

ArticleCarcinogenesis2008

Combined effects of the p53 codon 72 and p73 G4C14-to-A4T14 polymorphisms on the risk of HPV16-associated oral cancer in never-smokers.

Xingming Chen, Erich M Sturgis, Adel K El-Naggar, Qingyi Wei, Guojun Li

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 8 pooled it
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 8 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Association betweenThe Journal of international medical research · 2022
    Pooled it
  2. Bioscience reports · 2018
    Pooled it
  3. Pooled it
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  6. Association between the p53 codon 72 Arg/Pro polymorphism and hepatocellular carcinoma risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  7. No significant association between p53 codon 72 Arg/Pro polymorphism and risk of oral cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  8. Pooled it
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  15. Oncotarget · 2017
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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

5 authors at 2 institutions in 2 countries.

Xingming ChenDepartment of Head and Neck Surgery, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Erich M Sturgis
Adel K El-Naggar
Qingyi Wei
Guojun Li
The University of Texas MD Anderson Cancer Center · USPeking Union Medical College Hospital · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Paul A Scheet · 1985 to 2026
$290.8M
Targeting the p53 pathway for reversal of oral premalignancyP50CA097007 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MYERS, JEFFREY NICHOLAS · 2002 to 2012
$26.1M
Paul Calabresi Clinical Oncology AwardK12CA088084 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI David S. Hong, Scott Kopetz · 2000 to 2026
$14.0M
Molecular Epidemiology of Head and Neck CancerR01ES011740 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WEI, QINGYI · 2001 to 2012
$6.3M
Cytokine Variants as Predictors of HPV-16 Status & Outcome of Oropharyngeal CanceR03CA135679 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, GUOJUN · 2008 to 2009
$154k
NCI NIH HHS CA 135679NCI NIH HHS CA 16672NCI NIH HHS K-12 CA88084NCI NIH HHS P50 CA097007NIEHS NIH HHS ES 11740
6 · The paper itself

Abstract

Because p53 and p73 are associated with critical cellular processes and can be inactivated or degraded by the human papillomavirus (HPV) E6 oncoprotein, we investigated the combined effects of p53 codon 72 and p73 G4C14-to-A4T14 polymorphisms on the risk of HPV16-associated oral cancer. We analyzed genotype data from 326 patients with squamous cell carcinoma of the oral cavity or oropharynx and 349 cancer-free controls. We found that HPV16 seropositivity was associated with an increased risk of oral cancer [adjusted odds ratio (OR), 3.42; 95% confidence interval (CI), 2.28-5.13], especially among never-smokers (adjusted OR, 8.20; 95% CI, 3.66-18.4) and subjects with variant genotypes [adjusted OR for p53 Arg/Pro + Pro/Pro (Pro carriers), 5.00; 95% CI, 2.72-9.21; adjusted OR for p73 GC/AT + AT/AT (AT carriers), 3.83; 95% CI, 1.98-7.41]. HPV16 seropositivity was also associated with an significantly increased risk of oral cancer in all three risk groups with combined genotypes [adjusted ORs (95% CIs) were 2.28 (1.15-4.54) for p53 Arg/Arg and p73 GC/GC, the low-risk group; 3.97 (2.14-7.36) for p53 Arg/Arg and p73 AT carriers or p53 Pro carriers and p73 GC/GC, the medium-risk group and 5.11 (2.00-13.0) for p53 Pro carriers and p73 AT carriers, the high-risk group]. Moreover, HPV16-seropositive never-smokers in the high-risk group exhibited an approximately 11-fold greater risk of oral cancer (adjusted OR, 11.3; 95% CI, 1.22-106.0) than did HPV16-seronegative never-smokers in the low-risk group. These findings suggest that the combined variants of p53 and p73 significantly increase the risk of HPV16-associated oral cancer, especially among never-smokers.

Indexed as

CodonGenes, p53Polymorphism, GeneticAlphapapillomavirusBase SequenceCase-Control StudiesDNA-Binding ProteinsDNA PrimersHumansMouth NeoplasmsNuclear ProteinsSmokingTumor Protein p73Tumor Suppressor ProteinsCodonDNA-Binding ProteinsDNA PrimersNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID18701437
PMCPMC2577141
OpenAlexW2115519865

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.