Abstract
Gliomas account for almost 80 % of primary malignant brain tumors and are a major cause of morbidity and mortality more than any other tumor. The p53 gene is a tumor suppressor gene that plays a role in genomic stability, cell cycle control, and DNA repair after damage and apoptosis. Malfunction of the p53 pathway is a universal hallmark of human tumors with p53 codon 72 polymorphism reported to affect regulatory networks central to glioma development. The aim of work was to investigate the role of p53 Arg72Pro single nucleotide polymorphism (SNP) in the pathogenesis of gliomas and its effect on the serum level of p53. Forty-five glioma patients and 50 control subjects were included for whom genotyping for p53 Arg72Pro SNP by polymerase chain reaction-restriction fragment length polymorphism as well as measurement of serum p53 level were done. No statistically significant difference was observed in genotype distribution or allele frequency between cases and control and nor was there a significant difference in serum p53 level. In conclusion, in our work, no association was detected between p53 Arg72Pro SNP and the pathogenesis of gliomas, and neither was there an observed effect for the different genotypes on serum p53 levels.
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Gohar, N., Shehata, M., ElAbd, D. et al. Role of p53 Arg72Pro SNP in the pathogenesis of gliomas and its effect on serum level of p53. Comp Clin Pathol 23, 83–89 (2014). https://doi.org/10.1007/s00580-012-1574-7
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DOI: https://doi.org/10.1007/s00580-012-1574-7