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首页> 外文OA文献 >GSTM1 null and NAT2 slow acetylation genotypes, smoking intensity and bladder cancer risk: results from the New England bladder cancer study and NAT2 meta-analysis
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GSTM1 null and NAT2 slow acetylation genotypes, smoking intensity and bladder cancer risk: results from the New England bladder cancer study and NAT2 meta-analysis

机译：GSTM1 null和NAT2慢乙酰化基因型，吸烟强度和膀胱癌风险：新英格兰膀胱癌研究和NAT2荟萃分析的结果

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Associations between bladder cancer risk and NAT2 and GSTM1 polymorphisms have emerged as some of the most consistent findings in the genetic epidemiology of common metabolic polymorphisms and cancer, but their interaction with tobacco use, intensity and duration remain unclear. In a New England population-based case–control study of urothelial carcinoma, we collected mouthwash samples from 1088 of 1171 cases (92.9%) and 1282 of 1418 controls (91.2%) for genotype analysis of GSTM1, GSTT1 and NAT2 polymorphisms. Odds ratios and 95% confidence intervals of bladder cancer among New England Bladder Cancer Study subjects with one or two inactive GSTM1 alleles (i.e. the ‘null’ genotype) were 1.26 (0.85–1.88) and 1.54 (1.05–2.25), respectively (P-trend = 0.008), compared with those with two active copies. GSTT1 inactive alleles were not associated with risk. NAT2 slow acetylation status was not associated with risk among never (1.04; 0.71–1.51), former (0.95; 0.75–1.20) or current smokers (1.33; 0.91–1.95); however, a relationship emerged when smoking intensity was evaluated. Among slow acetylators who ever smoked at least 40 cigarettes/day, risk was elevated among ever (1.82; 1.14–2.91, P-interaction = 0.07) and current heavy smokers (3.16; 1.22–8.19, P-interaction = 0.03) compared with rapid acetylators in each category; but was not observed at lower intensities. In contrast, the effect of GSTM1-null genotype was not greater among smokers, regardless of intensity. Meta-analysis of the NAT2 associations with bladder cancer showed a highly significant relationship. Findings from this large USA population-based study provided evidence that the NAT2 slow acetylation genotype interacts with tobacco smoking as a function of exposure intensity.
机译：膀胱癌风险与NAT2和GSTM1多态性之间的关联已成为常见代谢多态性和癌症的遗传流行病学中一些最一致的发现，但它们与烟草使用，强度和持续时间的相互作用尚不清楚。在一项基于新英格兰人群的尿路上皮癌病例对照研究中，我们收集了1171例患者中的1088例（92.9％）和1418例对照中1282例（91.2％）的漱口水样本，用于GSTM1，GSTT1和NAT2多态性的基因型分析。具有一个或两个非活性GSTM1等位基因（即“无效”基因型）的新英格兰膀胱癌研究受试者的膀胱癌几率和95％置信区间分别为1.26（0.85–1.88）和1.54（1.05–2.25）（P -trend = 0.008），与具有两个有效副本的副本相比。 GSTT1无效等位基因与风险无关。 NAT2缓慢乙酰化状态与从未吸烟者（1.04; 0.71–1.51），以前吸烟者（0.95; 0.75–1.20）或当前吸烟者（1.33; 0.91–1.95）的风险无关。但是，在评估吸烟强度时出现了一种关系。在每天至少抽40支香烟的慢速乙酰化剂中，与以往相比，吸烟者（1.82； 1.14–2.91，P交互作用= 0.07）和目前大量吸烟者（3.16； 1.22–8.19，P交互作用= 0.03）的危险性均升高。每个类别中的快速乙酰化剂；但在较低强度下未观察到。相反，不管强度如何，吸烟者中GSTM1无效基因型的影响并不大。 NAT2与膀胱癌相关性的荟萃分析显示出高度重要的关系。这项基于美国人口的大型研究的发现提供了证据，即NAT2慢乙酰化基因型与吸烟相互作用，是暴露强度的函数。

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