环氧化酶-2启动子变异与幽门螺杆菌感染交互和食管癌发病风险的关系  

Genetic variants in the promoter of cyciooxygenase 2 interacting with Hp infection and the risk ofesophageal cancer

作　　者：张志[1] 王宏戈[2] 宋文广[1] 杨照环[1] 陈红[1] 王瑞林[1] 付占昭 

机构地区：[1]唐山市工人医院肿瘤放化疗科,河北省063000 [2]河北联合大学卫生学院流行病学教研室 [3]河北省秦皇岛市人民医院肿瘤放化疗科

出　　处：《中国综合临床》2011年第7期751-753,共3页Clinical Medicine of China

摘　　要：目的探讨环氧化酶-2（COX-2）启动子区遗传变异与食管癌发病风险的关系，并评价幽门螺杆菌（Hp）感染对其相互作用的影响。方法以PCR-限制性片断长度多态性方法在119例食管癌患者和238例健康对照中进行基因分型。以Logistic回归计算比值比（OR）和95％可信区间（CI）。结果COX-2启动子区一1195G〉A遗传变异和食管癌发病风险相关。与1195GG基因型携带者相比，1195GA基因型和1195AA基因型罹患食管癌的发病风险增高，其OR（95％CI）值分别为2．69（1．46～5．14）和2．30（1．23～4．89）。而且这种相关关系仅存在于Hp感染阳性的个体中，其OR（95％CI）值为2．74（1．35—5．96）。结论COX一2启动子区遗传变异对食管癌发病风险的影响和Hp感染的状态有关。Objective To evaluate the association of COX2 genetic variants with the risk of esophageal cancer and the interaction of COX2 genetic variants with Hp infection. Methods A total of 119 patients with esophageal cancer and 238 frequency-matched controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism method. Odds ratios （OR） and 95% confidence intervals （CI） were estim[tted by logistic regression. Results Case-control analysis showed an increased risk of developing esophageal cancer for 1195 GA （ OR = 2.69,95% CI = 1.46 - 5.14） and 1195AA （ OR = 2.30,95% C1 = 1.23 - 4.89） genotype carriers,respectively, compared with non 1195 GG carriers. When stratified by Hp status, the significantly increased risk of esophageal cancer was found among Hp carrier with OR （95% CI） =2.74 （ 1.35 -5.96） ,but not among Hp non-carriers. Conclusion Genetic polymorphism in COX2 promoter region may play an important role in esophageal cancer by Hp infection.

关 键 词：环氧化酶-2 食管癌 遗传变异 单核苷酸多态 

分 类 号：R735.1[医药卫生—肿瘤]