Genetic polymorphism of glutathione S-transferase P1 gene and lung cancer risk
Genetic polymorphism of glutathione S-transferase P1 gene and lung cancer risk
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DOI：
10.1023/a:1008811824890
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发表时间：
1999-02-01
影响因子：
2.3
通讯作者：
Corbella, J
中科院分区：
文献类型：
--
作者：
To-Figueras, J;Gené, M;Corbella, J
目的：人GSTTP 1基因具有多态性，第5外显子的A → G转换导致GSTP 1蛋白的10 5 Ile →瓦尔替换。分别由等位基因GST 1 *A和GST 1 *B编码的两种异构体对某些致癌环氧化物显示出不同的催化效率。在这项研究中，我们已经解决了可能的作用的Ile 105 Val GSTP 1多态性在肺癌susceptibility.Methods：多态性位点的基因分型在一组肺癌患者（n = 164）和两个对照组（健康吸烟者，n = 132;一般人群，n = 200）。所有患者和对照组西北地中海高加索人相同的种族origin.Results和结论：癌症患者显示的频率GST 1 *A/A，GST 1 *A/B和GST 1 *B/B（分别为50%，38%，11%）非常相似的两个对照组（健康吸烟者：48%，41%，11%）。在调整年龄、性别和吸烟状况后，未发现GST 1 *B等位基因与肺癌风险相关（OR：1.18; 95%CI：0.67-2.07）。结合GSTM 1和GSTT 1基因分析了Ile 105 val GSTP 1多态性。结果表明，GSTP 1等位基因并不增加与GSTM 1或GSTT 1缺失相关的风险。
Objectives: The human GSTTP1 gene is polymorphic with an A --> G transition in exon 5 causing a replacement 105 Ile --> Val in the GSTP1 protein. The two isoforms, encoded by the alleles GSTP1*A and GSTP1*B, respectively, show different catalytic efficiencies towards some carcinogenic epoxides. In this study we have addressed the possible role of the Ile105Val GSTP1 polymorphism in lung cancer susceptibility.Methods: The polymorphic site was genotyped by RFLP in a group of lung cancer patients (n = 164) and in two control groups (healthy smokers, n = 132; general population, n = 200). All patients and controls were Northwestern Mediterranean Caucasians of the same ethnic origin.Results and Conclusions: The cancer patients showed frequencies of GSTP1*A/A; GSTP1*A/B and GSTP1*B/B (50%, 38%, 11%, respectively) very similar to those of both control groups (healthy smokers: 48%, 41%, 11%). After adjusting for age, sex and smoking status, no association was found between the GSTP1*B allele and lung cancer risk (OR: 1.18; 95% CI: 0.67-2.07). The Ile105val GSTP1 polymorphism was also analysed in combination with the GSTM1 and GSTT1 genes. The results showed that allelism at GSTP1 did not increase the risk associated with the GSTM1 or GSTT1 deletions.