The First College of Clinical Medicine of Lanzhou University, Lanzhou 730000, Gansu Province, China.
World J Gastroenterol. 2010 Oct 7;16(37):4738-46. doi: 10.3748/wjg.v16.i37.4738.
To investigate the effects of superoxide dismutase (SOD) polymorphisms (rs4998557, rs4880), Helicobacter pylori (H. pylori) infection and environmental factors in gastric cancer (GC) and malignant potential of gastric precancerous lesions (GPL).
Copper-zinc superoxide dismutase (SOD1, CuZn-SOD)-G7958A (rs4998557) and manganese superoxide dismutase (SOD2, Mn-SOD)-Val16Ala (rs4880) polymorphisms were genotyped by SNaPshot multiplex polymerase chain reaction (PCR) in 145 patients with GPL (87 cases of gastric ulcer, 33 cases of gastric polyps and 25 cases of atrophic gastritis), 140 patients with GC and 147 healthy controls. H. pylori infection was detected by immunoblotting analysis.
The SOD1-7958A allele was associated with a higher risk of gastric cancer [odds ratio (OR) = 3.01, 95% confidence intervals (95% CI): 1.83-4.95]. SOD2-16Ala/Val genotype was a risk factor for malignant potential of GPL (OR = 2.04, 95% CI: 1.19-3.49). SOD2-16Ala/- genotype increased the risk of gastric cancer (OR = 2.85, 95% CI: 1.66-4.89). SOD1-7958A/- genotype, SOD2-16Ala/- genotype, alcohol drinking, positive family history and type I H. pylori infection were associated with risk of gastric cancer, and there were additive interactions between the two genotypes and the other three risk factors. SOD2-16Ala/Val genotype and positive family history were associated with malignant potential of GPL and jointly contributed to a higher risk for malignant potential of GPL (OR = 7.71, 95% CI: 2.10-28.22). SOD1-7958A/- genotype and SOD2-16Ala/- genotype jointly contributed to a higher risk for gastric cancer (OR = 6.43, 95% CI: 3.20-12.91).
SOD1-7958A/- and SOD2-16Ala/-genotypes increase the risk of gastric cancer in Chinese Han population. SOD2-16Ala/-genotype is associated with malignant potential of GPL.
探讨超氧化物歧化酶（SOD）多态性（rs4998557、rs4880）、幽门螺杆菌（H. pylori）感染和环境因素对胃癌（GC）和胃癌前病变（GPL）恶性潜能的影响。
采用 SNaPshot 多重聚合酶链反应（PCR）检测 145 例 GPL（87 例胃溃疡、33 例胃息肉和 25 例萎缩性胃炎）、140 例 GC 患者和 147 例健康对照者的铜锌超氧化物歧化酶（SOD1、CuZn-SOD）-G7958A（rs4998557）和锰超氧化物歧化酶（SOD2、Mn-SOD）-Val16Ala（rs4880）多态性。采用免疫印迹法检测 H. pylori 感染。
SOD1-7958A 等位基因与胃癌风险增加相关[比值比（OR）=3.01，95%置信区间（95%CI）：1.83-4.95]。SOD2-16Ala/Val 基因型是 GPL 恶性潜能的危险因素（OR=2.04，95%CI：1.19-3.49）。SOD2-16Ala/-基因型增加了胃癌的风险（OR=2.85，95%CI：1.66-4.89）。SOD1-7958A/-基因型、SOD2-16Ala/-基因型、饮酒、阳性家族史和Ⅰ型 H. pylori 感染与胃癌风险相关，且两种基因型与其他三个危险因素之间存在相加交互作用。SOD2-16Ala/Val 基因型和阳性家族史与 GPL 的恶性潜能相关，并共同导致 GPL 恶性潜能的风险增加（OR=7.71，95%CI：2.10-28.22）。SOD1-7958A/-基因型和 SOD2-16Ala/-基因型共同导致胃癌风险增加（OR=6.43，95%CI：3.20-12.91）。
中国汉族人群中 SOD1-7958A/-和 SOD2-16Ala/-基因型增加了胃癌的风险。SOD2-16Ala/-基因型与 GPL 的恶性潜能有关。
