AURKA rs8173 G>C Polymorphism Decreases Wilms Tumor Risk in Chinese Children.

Tongyi Lu,Li Li,Jiabin Liu,Ao Lin,Tiesong Zhang,Wen Fu,Guochang Liu,Jinhong Zhu,Huimin Xia,Jing He

doi:10.1155/2019/9074908

Abstract

Wilms tumor is the most common type of renal malignancy in children. Previous studies have demonstrated that single nucleotide polymorphisms (SNPs) in the AURKA gene could predispose to several human malignancies. We recruited 145 cases and 531 cancer-free controls to investigate whether AURKA gene variants modify Wilms tumor susceptibility. Three AURKA SNPs (rs1047972 C>T, rs2273535 T>A, and rs8173 G>C) were genotyped by the Taqman methodology. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of association between AURKA SNPs and Wilms tumor risk. We found that only the rs8173 G>C polymorphism was significantly associated with Wilms tumor risk (GC vs. GG: adjusted OR (AOR) = 0.50, 95% CI = 0.35–0.73, P=0.0002; GC/CC vs. GG: AOR = 0.60, 95% CI = 0.42–0.88, P=0.008). Stratification analysis revealed that rs8173 GC/CC genotypes were associated with Wilms tumor risk among children aged >18 months (AOR = 0.56, 95% CI = 0.34–0.93, P=0.024), male children (AOR = 0.54, 95% CI = 0.33–0.90, P=0.017), and children with clinical stage III + IV diseases (AOR = 0.56, 95% CI = 0.35–0.90, P=0.017). Haplotype analysis indicated that the CAG haplotype was significantly associated with increased Wilms tumor risk. In conclusion, our findings indicated that the AURKA rs8173 G>C polymorphism was associated with decreased Wilms tumor risk in Chinese children.

Highlights

Wilms tumor (WT), known as nephroblastoma, is the most common renal malignancy in children [1, 2]
Previous studies have found that genetic factors contribute to the risk of Wilms tumor and identified a number of genes associated with WT, including Wilms’ tumor protein 1 (WT1), β-catenin, tumor protein 53 (TP53), catenin beta 1 (CTNNB1), and AMER1 [11,12,13]
We found that carriers of rs8173 GC/CC genotypes had a decreased WT risk when compared with GG genotype carriers, among children older than 18 months (AOR 0.56, 95% confidence intervals (CIs) 0.34–0.93, P 0.024), male children (AOR 0.54, 95% CI 0.33–0.90, P 0.017), and those with the clinical stage III + IV diseases (AOR 0.56, 95% CI 0.35–0.90, P 0.017)

Summary

Introduction

Wilms tumor (WT), known as nephroblastoma, is the most common renal malignancy in children [1, 2]. It accounts for 6% to 7% of malignant tumors in children under the age of 15 years, with an incidence rate of about 7–10 cases per million in Western countries [3]. Previous studies have found that genetic factors contribute to the risk of Wilms tumor and identified a number of genes associated with WT, including Wilms’ tumor protein 1 (WT1), β-catenin, tumor protein 53 (TP53), catenin beta 1 (CTNNB1), and AMER1 [11,12,13]. Recent genome-wide studies on WT have revealed some previously unknown gene mutations implicated with WT, current known genetic variants are not adequate to fully elucidate the pathogenesis of WT [14]. erefore, it is Journal of Oncology important to identify more causal genetic variants for WT

Methods

Discussion

Conclusion