Joint effect of asthma/atopy and an IL-6 gene polymorphism on lung cancer risk among lifetime non-smoking Chinese women

• Published in: Carcinogenesis (New York) 2006-06, Vol.27 (6), p.1240-1244
• Main Authors: Seow, Adeline, Ng, Daniel PK, Choo, Serena, Eng, Philip, Poh, Wee-Teng, Ming, Teh, Wang, Yee-Tang
• Format: Article
• Language: English
• Subjects: Aged; Asthma - genetics; Asthma - metabolism; Asthma - pathology; Biological and medical sciences; Carcinogenesis, carcinogens and anticarcinogens; Case-Control Studies; China; Chronic obstructive pulmonary disease, asthma; confidence interval; Female; Genetic Predisposition to Disease; Humans; Hypersensitivity, Immediate - genetics; IL-6; Inflammation; interleukin-6; Interleukin-6 - genetics; Lung cancer; Lung Neoplasms - etiology; Lung Neoplasms - genetics; Medical sciences; Middle Aged; Odds Ratio; Pneumology; Polymorphism, Genetic; Smoking; Tumors; Tumors of the respiratory system and mediastinum
• ISSN: 0143-3334; 1460-2180
• DOI: 10.1093/carcin/bgi309

Recent evidence suggests that inflammatory pathways are important mediators of carcinogenesis. Asthma, allergic rhinitis and atopic dermatitis are clinical manifestations of a systemic atopic disorder, which is associated with airway hyper-responsiveness and inflammation. We examined the effect of a history of asthma/atopy among 132 lung cancer cases (of which 72% were adenocarcinomas) and 163 controls, all of whom were non-smoking Chinese women, in combination with a single nucleotide polymorphism (−634C/G) in the interleukin-6 (IL-6) gene which regulates secretion of a pro-inflammatory cytokine found to be predominant in lung tumour tissue. We observed a slight increase in risk of lung cancer [odds ratio, OR = 1.5, 95% confidence interval (95% CI) = 0.8–2.6] and of adenocarcinoma (OR = 1.6, 95% CI = 0.9–3.1) with asthma/atopy alone. There was no effect of the IL-6 CG/GG genotype on lung cancer risk on its own. Among individuals with both asthma/atopy and the IL-6 −634 G allele, however, risk was increased at least 3-fold (OR = 3.1, 95% CI = 1.2–8.3 for all cancers and OR = 4.2, 95% CI = 1.5–11.6 for adenocarcinomas) relative to individuals with no asthma/atopy and the CC genotype. On stratified analysis, a significant increase in risk with asthma/atopy was restricted to those with the at-risk genotype (Pint < 0.05). Our findings are consistent with the role of chronic inflammation as an aetiologic factor among non-smoking Asian women, and suggest that asthma/atopy is a risk marker for susceptibility to the development of lung cancer.