Abstract
BackgroundThe oxidative stress mechanism is of particular interest in the pathogenesis of glioma, given the high rate of oxygen metabolism in the brain. Potential links between polymorphisms of antioxidant genes and glioma risk are currently unknown. We therefore investigated the association between polymorphisms in antioxidant genes and glioma risk.MethodsWe examined 16 single nucleotide polymorphisms (SNPs) of 9 antioxidant genes (GPX1, CAT, PON1, NQO1, SOD2/MnSOD, SOD3, and NOS1*2*3) in 384 glioma and 384 control cases in a Chinese hospital-based case–control study. Genotypes were determined using the OpenArray platform, which employs the chip-based Taq-Man genotyping technology. The adjusted odds ratio (OR) and 95% confidence interval (CI) were estimated using unconditional logistic regression.ResultsUsing single-locus analysis, we identified four SNPs (SOD2 V16A, SOD3 T58A, GPX1 -46 C/T, and NOS1 3’-UTR) that were significantly associated with the risk of glioma development. To assess the cumulative effects, we performed a combined unfavourable genotype analysis. Compared with the reference group that exhibited no unfavourable genotypes, the medium- and high-risk groups exhibited a 1.86-fold (95% CI, 1.30-2.67) and a 4.86-fold (95% CI, 1.33-17.71) increased risk of glioma, respectively (P-value for the trend < 0.001).ConclusionsThese data suggest that genetic variations in oxidative stress genes might contribute to the aetiology of glioma.
Highlights
The oxidative stress mechanism is of particular interest in the pathogenesis of glioma, given the high rate of oxygen metabolism in the brain
Selection of genes and polymorphisms Through an extensive mining of the databases of the International HapMap Project (HapMap Data Rel 24/ phaseII Nov08) and dbSNP, we identified 16 potential functional polymorphisms, which were located within the 50-UTR, 30-UTR, promoter, coding sequence, and splice sites of nine crucial genes involved in oxidative stress response
Such antioxidant mechanisms are extremely important, as they represent the direct removal of reactive oxygen species (ROS)/reactive nitrogen species (RNS), during gliomatous carcinogenesis
Summary
The oxidative stress mechanism is of particular interest in the pathogenesis of glioma, given the high rate of oxygen metabolism in the brain. Potential links between polymorphisms of antioxidant genes and glioma risk are currently unknown. We investigated the association between polymorphisms in antioxidant genes and glioma risk. The incidence rate has steadily increased despite significant advances in the diagnosis and treatment of glioma [4]; The aetiology of this malignancy remains largely unknown. People with inherited diseases such as Li-Fraumeni disease, Neurofibromatosis type 1, and Turcot’s disease type 1 exhibit a significantly increased risk of glioma, and consistent with this diversity of predisposing genetic backgrounds, large-scale sequencing of the glioblastoma genome has revealed many genetic alterations [5,6]. There have been many relevant studies focused on the role of polymorphism analysis of candidate genes in glioma risk [7,8,9,10]. The evidence far provides us with important insight for our understanding of the aetiology of and susceptibility for gliomas
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