Abstract
Wilms tumor is the most common pediatric malignancy in the kidney. The miR34b/c is a downstream target gene of the transcription factor p53. The important role of TP53 mutations, the methylation of miR34b/c, and the interaction between these two molecules in tumorigenesis have been well documented. Due to the biological connection between p53 and miR34b/c, in the present study, we investigated the association between polymorphisms in these two molecules and Wilms tumor susceptibility through genotyping two important functional polymorphisms (miR34b/c rs4938723 T>C and TP53 rs1042522 C>G) in 183 cases and 603 controls. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) derived from the logistic regression analysis were used to assess the correlation of miR34b/c rs4938723 and TP53 rs1042522 polymorphisms with Wilms tumor risk. Our results indicated that the association of miR34b/c rs4938723 and TP53 rs1042522 polymorphisms with Wilms tumor susceptibility was not statistically significant. Stratified analysis by age, gender, and clinical stage, as well as combined effect analysis were also performed, yet, no significant association was found. In conclusion, our study indicated a lack of association between the two selected polymorphisms and Wilms tumor susceptibility. Our findings need to be verified in studies with larger sample size in the future.
Highlights
Wilms tumor, a malignant kidney tumor in children, currently has achieved a high survival rate in different geographical regions [1,2]
For miR34b/c rs4938723, the carriers with TC or CC genotypes showed no significant association with Wilms tumor risk compared with carriers of the TT genotype
For TP53 rs1042522, the carriers with CG or GG genotypes showed no significant association with Wilms tumor risk compared with carriers of the CC genotype
Summary
A malignant kidney tumor in children, currently has achieved a high survival rate in different geographical regions [1,2]. Molecular genetics studies showed that Wilms tumor had a complex etiology involving genetic lesions in the multiple sites [5,6]; and various gene polymorphisms play pivotal roles in the occurrence of Wilms tumor. There remain numerous functional single nucleotide polymorphisms (SNPs) in oncogenes and tumor suppressor genes, whose roles in Wilms tumor susceptibility need to be clarified. Gene mutation is a crucial factor in the tumorigenesis of Wilms tumor. Mutations in the coding sequence of the p53 gene were found in Wilms tumor patients by several research groups [7,8]. Apart from that, Slade et al [9] showed that translocation t(5;6)(q21;q21), leading to the inactivation of the HACE1 gene, predisposed Wilms tumor. Over the past decade, many genes have been found to be involved in the development of Wilms tumor, including MYCN [10], CTNNB1 [11], WTX [12], CHEK2 [6], BARD1 [13], hOGG1 and FEN1 gene [14] and KRAS [15]
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