TY - JOUR
T1 - IL1B rs1143634 polymorphism, cigarette smoking, alcohol use, and lung cancer risk in a Japanese population
AU - Kiyohara, Chikako
AU - Horiuchi, Takahiko
AU - Takayama, Koichi
AU - Nakanishi, Yoichi
N1 - Funding Information:
Supported by a Grant-in-Aid for Scientific Research (B) (2139019) from the Ministry of Education, Science, Sports and Culture, Japan.
PY - 2010/3
Y1 - 2010/3
N2 - 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.
AB - 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.
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U2 - 10.1097/JTO.0b013e3181c8cae3
DO - 10.1097/JTO.0b013e3181c8cae3
M3 - Article
C2 - 20035239
AN - SCOPUS:77649327816
VL - 5
SP - 299
EP - 304
JO - Journal of Thoracic Oncology
JF - Journal of Thoracic Oncology
SN - 1556-0864
IS - 3
ER -