Abstract

BackgroundThere are different and inconsistent conclusions regarding the genetic relationship between the human tumor suppressor p53 (TP53) rs1042522 polymorphism and the risk of oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL). Therefore, the aim of the study was to comprehensively reassess this association through the performance of an updated meta-analysis.MethodsAfter searching the available databases, we systematically screened and included the eligible case-control studies, which contain the full genotype frequency data of the TP53 rs1042522 polymorphism for both OSCC/OL patients and the negative control groups. PA (P-value of the association test) and ORs (odd ratios) with their corresponding 95% CIs (confidence intervals) were calculated to quantitatively evaluate the influence of TP53 rs1042522 on the susceptibility of patients to OSCC or OL.ResultsIn total, twenty eligible case-control articles were finally enrolled. Compared with the controls, no increased or decreased risk of OSCC was observed in the cases for six genetic models including allele C vs. G (PA = 0.741), carrier C vs. G (PA = 0.853), homozygote CC vs. GG (PA = 0.085), heterozygote GC vs. GG (PA = 0.882), dominant GC + CC vs. GG (PA = 0.969), and recessive CC vs. GG + GC (PA = 0.980). Furthermore, no statistically significant difference between the cases and controls was detected in most subgroup meta-analyses (PA > 0.05). For the risk of OL, we did not observe the difference between the cases and controls for most genetic models in the overall meta-analysis and subsequent subgroup analysis (PA > 0.05). Begg’s test and Egger’s test excluded the large risk of publication bias within the included studies in the meta-analysis of OSCC. The sensitivity analysis indicated the above relatively stable results.ConclusionsOur updated meta-analysis (based on the current evidence) shows that TP53 rs1042522 may not confer susceptibility to OSCC. In addition, for the first time, we provided evidence regarding the negative association between TP53 rs1042522 and OL risk.

Highlights

  • There are different and inconsistent conclusions regarding the genetic relationship between the human tumor suppressor p53 (TP53) rs1042522 polymorphism and the risk of oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL)

  • After screening the titles and abstracts, 114 records were excluded for various reasons: animal or cell data, other disease or unconfirmed OSCC (n = 31); other genes, other variants or an unconfirmed TP53 mutation site (n = 35); lack of a control group or full genotype frequency data in both the case and the control group (n = 21); metaanalysis, review, and meeting abstracts (n = 27)

  • In this study, we focused on the potential role of TP53 rs1042522 in the risk of oral squamous cell carcinoma through a meta-analysis of sixteen case-control studies

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Summary

Introduction

There are different and inconsistent conclusions regarding the genetic relationship between the human tumor suppressor p53 (TP53) rs1042522 polymorphism and the risk of oral squamous cell carcinoma (OSCC) and oral leukoplakia (OL). The rs1042522 G/C, which is a very common polymorphism at exon 4 of the TP53 gene, results in the alteration at codon 72 between arginine (Arg, R) and proline (Pro, P) and causes the TP53Arg72Pro mutation. This may affect the normal function of the TP53 protein and is implicated in susceptibility to several clinical diseases (e.g., colorectal cancer [4], endometriosis [5] or type 2 diabetes [6]). Life style (e.g., tobacco smoking, drinking, and chewing), human papillomavirus (HPV) infection, and other functional variants may be implicated in the etiology of OSCC and OL [7,8,9]

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