CAT, GPX1, MnSOD, GSTM1, GSTT1, andGSTP1Genetic Polymorphisms in Chronic Myeloid Leukemia: A Case-Control Study

Abstract

Oxidative damage at the DNA level may be promoted by high levels of reactive oxygen species (ROS), leading to genomic instability and increased neoplastic risk. Superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) enzymes are implicated in the prevention of DNA damage by ROS. The aim of the study was to investigate the relationships betweenCATC262T,GPX1Pro198Leu,MnSODAla16Val,GSTM1, GSTT1, andGSTP1Ile105Val polymorphisms and the risk of CML. No association was observed between CML and variant genotypes ofGPX1, MnSOD, GSTM1, andGSTT1polymorphisms in any of the investigated cases. Our study suggests that the homozygous variant genotype of theGSTP1Ile105Val gene polymorphisms may be associated with the risk of developing CML (OR=2.5; 95% CI=1.08–5.7;Pvalue = 0.02), while the heterozygous genotype of theCATC262T polymorphism seems to have a protective effect against CML (OR=0.59, 95% CI=0.39–0.89,Pvalue = 0.01). In most cases, no association was found between laboratory parameters and prognostic factors and the variant genotype of investigated gene polymorphisms. We concluded thatCAT, GPX, MnSOD, GSTM1, andGSTT1gene polymorphisms are not associated with the risk of CML. Variant genotype of theGSTP1Ile105Val gene polymorphisms may contribute to the risk of developing CML.