The TP53 gene rs1042522 C>G polymorphism and neuroblastoma risk in Chinese children

TP53, a tumor suppressor gene, plays a critical role in cell cycle control, apoptosis, and DNA damage repair. Previous studies have indicated that the TP53 gene Arg72Pro (rs1042522 C>G) polymorphism is associated with susceptibility to various types of cancer. We evaluated the association of the TP53 gene rs1042522 C>G polymorphism with neuroblastoma susceptibility in a hospital-based study among the Chinese Han population. Enrolled were 256 patients and 531 controls. Odds ratios (ORs) and 95% confidence intervals (CIs) generated using logistic regression models were used to determine the strength of the association of interest. No association was detected between rs1042522 C>G polymorphism and neuroblastoma risk. In our stratification analysis of age, gender, sites of origin, and clinical stages, we observed that subjects with rs1042522 CG/GG genotypes had a lower risk of developing neuroblastoma in the mediastinum (Adjusted OR=0.52, 95% CI=0.33-0.82, P=0.005) than those carrying the CC genotype. These results indicate that TP53 gene rs1042522 C>G polymorphism may exert a weak and site-specific effect on neuroblastoma risk in Southern Chinese children and warrant further confirmation.

[1]  A. Fersht,et al.  Rescuing the function of mutant p53 , 2001, Nature Reviews Cancer.

[2]  H. Xia,et al.  Lack of Associations between XPC Gene Polymorphisms and Neuroblastoma Susceptibility in a Chinese Population , 2016, BioMed research international.

[3]  H. Xia,et al.  Potentially functional polymorphisms in the LIN28B gene contribute to neuroblastoma susceptibility in Chinese children , 2016, Journal of cellular and molecular medicine.

[4]  B. Mittal,et al.  Candidate gene studies in gallbladder cancer: a systematic review and meta-analysis. , 2011, Mutation research.

[5]  M. L. Belli,et al.  The p 53 Codon 72 Pro / Pro Genotype Identifies Poor-Prognosis Neuroblastoma Patients : Correlation with Reduced Apoptosis and Enhanced Senescence by the p 53-72 P Isoform 1 , 2 , 2012 .

[6]  Hua Tan,et al.  Genome-wide mutational spectra analysis reveals significant cancer-specific heterogeneity , 2015, Scientific Reports.

[7]  Xiaobo Zhou,et al.  A novel missense-mutation-related feature extraction scheme for 'driver' mutation identification , 2012, Bioinform..

[8]  C. Prives,et al.  Blinded by the Light: The Growing Complexity of p53 , 2009, Cell.

[9]  K K Matthay,et al.  Treatment of High-Risk Neuroblastoma with Intensive Chemotherapy, Radiotherapy, Autologous Bone Marrow Transplantation, and 13-cis-Retinoic Acid , 1999 .

[10]  H. Xia,et al.  LMO1 gene polymorphisms contribute to decreased neuroblastoma susceptibility in a Southern Chinese population , 2016, Oncotarget.

[11]  J. Levine,et al.  Surfing the p53 network , 2000, Nature.

[12]  T. Trikalinos,et al.  Genotype misclassification in genetic association studies of the rs1042522 TP53 (Arg72Pro) polymorphism: a systematic review of studies of breast, lung, colorectal, ovarian, and endometrial cancer. , 2013, American journal of epidemiology.

[13]  H. Xia,et al.  Evaluation of GWAS-identified SNPs at 6p22 with neuroblastoma susceptibility in a Chinese population , 2016, Tumor Biology.

[14]  Zhong-tao Zhang,et al.  Genetic association of single nucleotide polymorphisms in P53 pathway with gastric cancer risk in a Chinese Han population , 2014, Medical Oncology.

[15]  S. Altekruse,et al.  Outcomes for children and adolescents with cancer: challenges for the twenty-first century. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[16]  R. Schneider-Stock,et al.  Homozygous proline at codon 72 of p53 as a potential risk factor favoring the development of undifferentiated thyroid carcinoma. , 2002, International journal of oncology.