Association between p53 polymorphism at codon 72 and recurrent spontaneous abortion.
10.1007/s11596-016-1599-2
- Author:
Ying ZHANG
1
;
Yuan-Yuan WU
1
;
Fu-Yuan QIAO
1
;
Wan-Jiang ZENG
2
Author Information
1. Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
2. Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. wjzeng@tjh.tjmu.edu.cn.
- Publication Type:Journal Article
- Keywords:
codon 72;
gene polymorphism;
meta-analysis;
p53;
recurrent spontaneous abortion
- MeSH:
Abortion, Spontaneous;
diagnosis;
ethnology;
genetics;
physiopathology;
Adult;
Alleles;
Asian Continental Ancestry Group;
Case-Control Studies;
Codon;
European Continental Ancestry Group;
Female;
Gene Frequency;
Genetic Predisposition to Disease;
Humans;
Odds Ratio;
Polymorphism, Single Nucleotide;
Pregnancy;
Recurrence;
Risk Factors;
Tumor Suppressor Protein p53;
genetics;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(3):402-405
- CountryChina
- Language:English
-
Abstract:
p53 gene plays an important role in apoptosis, which is necessary for successful invasion of trophoblast cells. The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA). In order to investigate the association between p53 polymorphism at codon 72 and RSA, we conducted this meta-analysis. Pubmed, Embase and Web of science were used to identify the eligible studies. Odds ratio (OR) with 95% confidence interval (CI) was used to evaluate the strength of the association. Six studies containing 937 cases of RSA and 830 controls were included, and there was one study deviated from Hardy-Weinberg equilibrium (HWE). There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not. A significant association was observed in allelic model (Pro vs. Arg; OR=1.28, 95% CI: 1.04-1.57) after exclusion of the study that was deviated from HWE. No association was noted in recessive model (Pro/Pro+Pro/Arg vs. Arg/Arg; OR=1.05, 95% CI: 0.86-1.30) and co-dominant model (Pro/Arg vs. Arg/Arg; OR=0.96, 95% CI: 0.77-1.19). Subgroup analysis by ethnicity also indicated a significant association between p53 polymorphism at codon 72 and RSA in Caucasian group. No heterogeneity and publication bias were found. Our meta-analysis implied that p53 polymorphism at codon 72 carries high maternal risk of RSA.
