SynthesisMedical oncology (Northwood, London, England)2011
TP53 Arg72Pro polymorphism and endometrial cancer risk: a meta-analysis.
Synthesis in Medical oncology (Northwood, London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparative study and meta-analysis of meta-analysis studies for the correlation of genomic markers with early cancer detection.Human genomics · 2013Pooled it
- The Expression Levels of XLF and Mutant P53 Are Inversely Correlated in Head and Neck Cancer Cells.Journal of Cancer · 2016Article
- Detection of human papillomavirus (HPV) DNA prevalence and p53 codon 72 (Arg72Pro) polymorphism in prostate cancer in a Greek group of patients.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Assessment of the XPC (A2920C), XPF (T30028C), TP53 (Arg72Pro) and GSTP1 (Ile105Val) polymorphisms in the risk of cutaneous melanoma.Journal of cancer research and clinical oncology · 2013Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies investigating the relationship between TP53 Arg72Pro polymorphism and endometrial cancer risk reported conflicting results. To explore a more precise estimate of the effect of this polymorphism on endometrial carcinogenesis, a meta-analysis was performed by searching eligible studies in PubMed. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association for codominant model (Arg/Arg vs. Pro/Pro, Arg/Pro vs. Pro/Pro), dominant model (Arg/Arg+Arg/Pro vs. Pro/Pro), and recessive model (Arg/Arg vs. Arg/Pro+Pro/Pro), respectively. Subgroup analyses were performed by Hardy-Weinberg equilibrium (HWE) in controls, the specimen of cases for determining TP53 genotypes, sample size, the source of control and case groups, and ethnicity. We identified 8 case-control studies involving 2,154 subjects for this meta-analysis. Overall, no evidence of association was observed between TP53 genotypes and endometrial cancer risk in all genetic models (Arg/Arg vs. Pro/Pro: OR=0.98, 95% CI: 0.69-1.39, P=0.90; Arg/Pro vs. Pro/Pro: OR=1.00, 95% CI: 0.71-1.42, P=0.98; dominant model: OR=0.99, 95% CI: 0.71-1.38, P=0.95; recessive model: OR=1.06, 95% CI: 0.80-1.41, P=0.95). Stratified analyses also detected no significant association in any subgroup, except among those studies with controls deviated from HWE in recessive model (OR=1.60, 95% CI: 1.07-2.39). In conclusion, we did not observe any evidence for a role of TP53 Arg72Pro polymorphism in endometrial cancer. The reported significant association between this polymorphism and endometrial cancer risk may be due to methodological errors such as selection bias, small sample size, Type I error, and population stratification.
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