Lack of associations between AURKA gene polymorphisms and neuroblastoma susceptibility in Chinese children.

Jue Tang,Jing He,Yuanmin Qian,Feng-Hua Wang,Jia-Hang Zeng,Jiang-Hua Liang,Jiao Zhang,Wei Liu,Jinhong Zhu,Huimin Xia,Hui Wang

doi:10.1042/bsr20180292

Abstract

Previous studies have demonstrated that polymorphisms in the AURKA gene are associated with various types of cancer. In neuroblastoma, AURKA protein product regulates N-myc protein levels and plays a critical role in tumorigenesis. To investigate the association between three AURKA polymorphisms (rs1047972 C>T, rs2273535 T>A, and rs8173 G>C) and neuroblastoma susceptibility in Chinese populations, we performed this two-center case–control study including 393 neuroblastoma cases and 812 controls. Two study populations were recruited from two different regions in China. No significant associations were identified amongst any of the three AURKA polymorphisms and the risk of neuroblastoma. Similar observations were found in the stratified analysis. In conclusion, our results indicate that none of the AURKA polymorphisms are associated with neuroblastoma susceptibility in two distinct Chinese populations. Further studies with larger sample sizes and different ethnicities are warranted to validate our results.

Highlights

Neuroblastoma is a neuroendocrine tumor that originates from the developing sympathetic nervous system
We conducted the present case–control study with a total of 393 neuroblastoma patients and 812 control subjects to investigate the impact of three AURKA single nucleotide polymorphism (SNP) on the risk of neuroblastoma in Chinese populations
Our data indicated that none of the selected SNPs were associated with neuroblastoma susceptibility in two independent Chinese populations

Summary

Introduction

Neuroblastoma is a neuroendocrine tumor that originates from the developing sympathetic nervous system. It is the most common solid malignancy in the first year of life, accounting for approximately 15% of pediatric cancer deaths [1]. Genetic variations have been shown to be important factors in the origination and development of neuroblastoma [3,4,5]. A previous genome-wide association study (GWAS) demonstrated that common genetic variations in the BARD1 gene may contribute to the etiology of the aggressive neuroblastoma [6]. Single nucleotide polymorphisms (SNPs) within DDX4, HSD17B12, and DUSP12 are recurrent in low-risk neuroblastoma [11,12]. Previous study demonstrated that LIN28B promotes AURKA expression via inhibition of let-7, further driving neuroblastoma oncogenesis [15]

Methods

Results

Conclusion