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白细胞介素 1B(rs1143634) 多态性、吸烟、饮酒与日本人群肺癌风险的关系。

IL1B rs1143634 polymorphism, cigarette smoking, alcohol use, and lung cancer risk in a Japanese population.

机构信息

Department of Preventive Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan.

出版信息

J Thorac Oncol. 2010 Mar;5(3):299-304. doi: 10.1097/JTO.0b013e3181c8cae3.

DOI:10.1097/JTO.0b013e3181c8cae3
PMID:20035239
Abstract

BACKGROUND

Interleukin 1B (IL1B) is involved in pulmonary inflammation induced by environmental or occupational toxins. Chronic inflammation has been implicated in the development of lung cancer.

METHODS

We evaluated the role of IL1B (rs1143634, 3954C>T) in a case-control study comprised of 462 lung cancer cases and 379 controls in a Japanese population. Logistic regression was used to assess the adjusted odds ratios (OR) and 95% confidence intervals (95% CI).

RESULTS AND DISCUSSION

Individuals with a history of smoking and at least one T allele (adjusted OR = 5.45, 95% CI = 2.75-4.42, p < 0.01) presented a higher risk of lung cancer than those with the CC genotype (adjusted OR = 2.86, 95% CI = 2.02-4.05, p < 0.01) as compared with never smokers with the CC genotype (reference). The adjusted attributable proportion because of interaction between the IL1B rs1143634 genotypes and smoking was estimated to be 0.45 (95% CI = 0.08-0.83, p = 0.02), indicating that 45% of the excess risk for lung cancer in ever smokers with at least one T allele was due to additive interaction. Subjects with excessive alcohol intake and at least one T allele had a significantly higher risk (OR = 2.48, 95% CI =1.36-4.54, p < 0.01) than drinkers with appropriate intake and the CC genotype. There was no interaction between the polymorphism and alcohol intake.

CONCLUSIONS

Our findings indicate the possible association of the T allele carriers of the IL1B rs1143634 polymorphism with higher risk of lung cancer especially among smokers. Additional studies are warranted to confirm the IL1B rs1143634-smoking interaction suggested in this study.

摘要

背景

白细胞介素 1B(IL1B)参与环境或职业毒素引起的肺部炎症。慢性炎症与肺癌的发展有关。

方法

我们在一个日本人群中进行了病例对照研究,包括 462 例肺癌病例和 379 例对照,评估了 IL1B(rs1143634,3954C>T)的作用。使用逻辑回归评估调整后的比值比(OR)和 95%置信区间(95%CI)。

结果与讨论

与从不吸烟者的 CC 基因型(参照)相比,有吸烟史且至少携带一个 T 等位基因的个体(调整 OR = 5.45,95%CI = 2.75-4.42,p < 0.01)患肺癌的风险更高,与从不吸烟者的 CC 基因型相比(调整 OR = 2.86,95%CI = 2.02-4.05,p < 0.01)。IL1B rs1143634 基因型与吸烟之间相互作用的调整归因比例估计为 0.45(95%CI = 0.08-0.83,p = 0.02),这表明,在至少携带一个 T 等位基因的吸烟者中,45%的肺癌超额风险归因于相加性相互作用。有过量饮酒史且至少携带一个 T 等位基因的个体患肺癌的风险显著更高(OR = 2.48,95%CI = 1.36-4.54,p < 0.01),与适量饮酒且携带 CC 基因型的个体相比。该多态性与饮酒之间没有相互作用。

结论

我们的研究结果表明,白细胞介素 1B(rs1143634)多态性的 T 等位基因携带者与肺癌风险增加之间可能存在关联,尤其是在吸烟者中。需要进一步的研究来证实本研究中提示的 IL1B rs1143634-吸烟相互作用。

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