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CAT GPX1 MnSOD GSTM1 GSTT1 and GSTP1 Genetic Polymorphisms in Chronic Myeloid Leukemia: A Case-Control Study

机译:慢性粒细胞白血病中CATGPX1MnSODGSTM1GSTT1和GSTP1遗传多态性的病例对照研究

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摘要

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 between CAT C262T, GPX1 Pro198Leu, MnSOD Ala16Val, GSTM1, GSTT1, and GSTP1 Ile105Val polymorphisms and the risk of CML. No association was observed between CML and variant genotypes of GPX1, MnSOD, GSTM1, and GSTT1 polymorphisms in any of the investigated cases. Our study suggests that the homozygous variant genotype of the GSTP1 Ile105Val gene polymorphisms may be associated with the risk of developing CML (OR = 2.5; 95% CI = 1.08–5.7; P value = 0.02), while the heterozygous genotype of the CAT C262T polymorphism seems to have a protective effect against CML (OR = 0.59, 95% CI = 0.39–0.89, P value = 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 that CAT, GPX, MnSOD, GSTM1, and GSTT1 gene polymorphisms are not associated with the risk of CML. Variant genotype of the GSTP1 Ile105Val gene polymorphisms may contribute to the risk of developing CML.
机译:高水平的活性氧(ROS)可能会促进DNA水平的氧化损伤,从而导致基因组不稳定和增生的肿瘤风险。超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GPX)和过氧化氢酶(CAT)酶与防止ROS引起的DNA损伤有关。该研究的目的是研究CAT C262T,GPX1 Pro198Leu,MnSOD Ala16Val,GSTM1,GSTT1和GSTP1 Ile105Val多态性与CML风险之间的关系。在任何调查的病例中,均未观察到CML与GPX1,MnSOD,GSTM1和GSTT1多态性的变异基因型之间的关联。我们的研究表明,GSTP1 Ile105Val基因多态性的纯合子基因型可能与发生CML的风险有关(OR = 2.5; 95%CI = 1.08-5.7; P值= 0.02),而CAT C262T的杂合子基因型多态性似乎对CML具有保护作用(OR = 0.59,95%CI = 0.39–0.89,P值= 0.01)。在大多数情况下,实验室参数和预后因素与所研究基因多态性的变异基因型之间没有关联。我们得出结论,CAT,GPX,MnSOD,GSTM1和GSTT1基因多态性与CML的风险无关。 GSTP1 Ile105Val基因多态性的变异基因型可能有助于发展CML。

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