Department of Molecular Biology and Genetics, Faculty of Science, Cumhuriyet University, 58140 Sivas, Turkey.
Mol Med Rep. 2011 Jan-Feb;4(1):87-92. doi: 10.3892/mmr.2010.378. Epub 2010 Oct 5.
Myeloperoxidase (MPO) is a phase I enzyme that can bioactivate many specific procarcinogens, including polycyclic aromatic hydrocarbons and aromatic amines. The MPO gene contains a common single nucleotide polymorphism, for which the -463G>A substitution within the promoter region has been shown to reduce MPO expression and activity. We investigated the association between the MPO -463G>A polymorphism and lung and prostate cancer in a Turkish population. MPO genotypes in the study populations were determined using polymerase chain reaction-based restriction fragment length polymorphism assay. The allelic frequency was significantly different between the cases and controls for lung cancer (p=0.02), but not prostate cancer (p=0.30). No significant difference was noted between the lung and prostate cancer cases and control populations in terms of genotype distribution (p=0.07, p=0.53, respectively). Control groups of lung and prostate cancer were in Hardy-Weinberg equilibrium (p=0.87 and p=0.41, respectively). To determine the protective effect against lung cancer among individuals with the -463A allele, G/A and A/A genotypes were combined. Comparison of the G/G and G/A + A/A genotypes between the lung cancer cases and control groups showed a statistically significant relationship (p=0.032, OR=0.60, 95% CI 0.38-0.95). No gender-specific difference was found in terms of genotype distribution between the lung cancer patients and the controls (female, p=0.20; male, p=0.34). In the case of smokers, a difference in genotype distribution between the lung cancer patients and the controls was statistically significant (p=0.02), although this difference was not statistically significant for non-smokers (p=0.90). Overall, no statistically significant difference was found between the prostate cancer cases and the controls in terms of genotype combination (p=0.46, OR=0.83, 95% CI 0.51-1.36). Additionally, in smokers and non-smokers, no significant relationship was determined between the prostate cancer patients and the control population (p=0.21, p=0.91, respectively). These results suggest that the MPO -463A allele significantly contributes to a protective effect overall and in smokers against lung cancer.
髓过氧化物酶 (MPO) 是一种 I 相酶，可使许多特定的前致癌物质生物活化，包括多环芳烃和芳香胺。MPO 基因含有一个常见的单核苷酸多态性，其启动子区域内的 -463G>A 取代已被证明可降低 MPO 的表达和活性。我们在土耳其人群中研究了 MPO -463G>A 多态性与肺癌和前列腺癌之间的关系。使用聚合酶链反应 - 基于限制片段长度多态性分析的研究人群中的 MPO 基因型。等位基因频率在病例和对照组之间对肺癌有显著差异（p=0.02），但对前列腺癌无差异（p=0.30）。在肺癌和前列腺癌病例和对照组的基因型分布方面，没有观察到显著差异（p=0.07，p=0.53）。肺癌和前列腺癌对照组均处于哈迪-温伯格平衡（p=0.87 和 p=0.41）。为了确定 -463A 等位基因个体对肺癌的保护作用，将 G/A 和 A/A 基因型合并。与对照组相比，肺癌病例中 G/G 和 G/A+A/A 基因型的比较显示出统计学上的显著关系（p=0.032，OR=0.60，95%CI 0.38-0.95）。在肺癌患者和对照组中，没有发现性别特异性的基因型分布差异（女性，p=0.20；男性，p=0.34）。对于吸烟者，肺癌患者和对照组之间的基因型分布差异具有统计学意义（p=0.02），但对于不吸烟者，这种差异无统计学意义（p=0.90）。总体而言，在前列腺癌病例和对照组之间，基因型组合无统计学差异（p=0.46，OR=0.83，95%CI 0.51-1.36）。此外，在吸烟者和不吸烟者中，前列腺癌患者与对照组之间未确定显著关系（p=0.21，p=0.91）。这些结果表明，MPO -463A 等位基因总体上以及在吸烟者中对肺癌具有显著的保护作用。
