吸烟影响IL1B基因多态与NSCLC易感性  

Smoking affected the association between IL1B gene polymorphisms and the risks of NSCLC

作　　者：李亚南[1] 赵维[1] 赵振宏[1] 陈林颀 吴俊杰[1,2] 李强[2] 卢大儒[1] 金力[1,3] 王久存[1,3] 

机构地区：[1]复旦大学生命科学学院现代人类学教育部重点实验室和遗传工程国家重点实验室,上海200433 [2]上海第二军医大学附属长海医院呼吸内科,200433 [3]复旦大学泰州健康科学研究院,泰州225300

出　　处：《国际遗传学杂志》2015年第1期1-8,13,共9页International Journal of Genetics

基　　金：国家科技支撑重点项目（2011BA109800）;国家高技术研究发展计划（2012AA021802）;国家自然科学基金（81372236）,上海市博士后科研资助面上项目（12R21411500）

摘　　要：目的探讨吸烟与IL1B基因多态性、非小细胞肺癌（NSCLC）遗传易感性之间的关系。方法本文采用病例-对照研究，对889例肺癌患者和1005例性别、年龄与之相匹配的健康对照中IL1B rs 1143623 G〉C和rs12621220 G〉A两个单核苷酸多态性位点（SNP）进行基因分型，并统计分析各基因型频率分布、吸烟与NSCLC患病的关系。结果①吸烟影响NSCLC易感性：有吸烟史的人群NSCLC患病风险较无吸烟史的人群高（校正性别、年龄、吸烟量等因素后，OR=3．744，95％CI=2．885～4．858；P=2．980×10^-22）；对有吸烟史的人群分析后发现高吸烟量增加NSCLC的风险（P=4．350×10^29）；进一步发现戒烟人群的吸烟量显著高于持续吸烟人群的吸烟量（P=0．016），持续吸烟但低吸烟量对NSCLC易感性有显著保护作用（校正性别、年龄、吸烟量等因素后，OR=0．219，95％CI=0．164～0．291；P=2．233×10^-25），即高吸烟量增加NSCLC风险；②吸烟因素影响IL1B rs 1143623 G〉C和rs 12621220G〉A与NSCLC易感性的关联：在戒烟人群中，rs1143623G〉C位点GC基因型对NSCLC发生具有较低限度的保护效应（校正性别、年龄、吸烟量等因素后，OR=0．543，95％CI=0．291～1．011；P=0．054），该种保护作用相对稳固，表现为联合GC＋CC基因型仍然对NSCLC有保护作用（校正OR=0．563，95％CI=0．313～1．013；P=0．055），进一步亚组分析发现，此种保护效应主要体现在对腺癌（ADC）的保护（校正OR=0．491，95％CI=0．241～1．001；P=0．050）；rs 12621220 G〉A位点GA基因型对NSCLC发生具有保护效应（校正OR=0．427，95％CI=0．210—0．868；P：0．019），此种保护效应主要是与ADC相关．结论儿，占某因多杰件与NSCLC易感性和吸烟行为相关。Objective The purpose of this study was to explore the association among IL1B polymorphisms, smoking and the risks of non-small cell lung cancer. Methods ILIB polymorphisms （ rs1143623G 〉 A, rs12621220G 〉 C ） were genotyped in 889 non-small cell lung cancer （ NSCLC ）cases and 1005 healthy controls. Results The results showed that smoking affected NSCLC susceptibility ： People with smoking history have much higher risk of NSCLC than people without smoking history （ after adjustment for factors, such as gender, age, pack-year, OR = 3.744, 95% CI = 2.885 4. 858 ; P = 2. 980 × 10^-23 ） ; Furthermore, people with higher smoking pack-years have much higher risk of NSCLC than those with lower smoking pack-years （ P = 4. 350 × 10^-29 ） , and the persistent smokers who smoked lower pack-years, has significant protective effect on NSCLC susceptibility （ aOR = 0.219, 95% CI =0. 164-0.291; P=2.233 × 10^-25） than the people quitted smoking but smoked more pack-years （P = 0. 016 ）. In addition, we found that the associations between NSCLC susceptibility and ILI B polymorphisms was influenced by smoking status. The logistic regression analysis results showed that： For rs1143623, compared with the GG genotype, GC was significantly associated with decreased risk of NSCLC for the people of smoking cessation （aOR = 0.543, 95% CI =0.291 - 1.011; P= 0. 054） , and this protection was relatively stable when combined with CC genotype （ aOR = 0. 563 , 95% CI =0.313 - 1.013; P=0.055）. In subgroups analysis we found that this protective effect was mainly existed in the subgroup ofadenocarcinoma （ADC） （OR=0.491, 95% CI =0.241 - 1.001; P = 0. 050 ） . For rs 12621220, compared with the GG genotype, GA was significantly associated with decreased risk of NSCLC ior the people of smoking cessation （OR = 0. 427, 95% CI = 0. 210 0. 868 ; P = 0. 019 ） , and this protective effect was mainly related to the ADC, combined with AA genotype, the protective effect did not disappear （OR = 0. 479, 95%

关 键 词：IL1B 单核苷酸多态性 吸烟 非小细胞肺癌 

分 类 号：R734.2[医药卫生—肿瘤]