title: Joint effect of asthma/atopy and an IL-6 gene polymorphism on lung cancer risk among lifetime non-smoking Chinese women.
abstract: 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.
authors.affiliation: Department of Community, Occupational and Family Medicine, National University of Singapore, Singapore. cofseowa@nus.edu.sg
authors.forename: Adeline
authors.initials: A
authors.lastname: Seow
authors.forename: Daniel Pk
authors.initials: DP
authors.lastname: Ng
authors.forename: Serena
authors.initials: S
authors.lastname: Choo
authors.forename: Philip
authors.initials: P
authors.lastname: Eng
authors.forename: Wee-Teng
authors.initials: WT
authors.lastname: Poh
authors.forename: Teh
authors.initials: T
authors.lastname: Ming
authors.forename: Yee-Tang
authors.initials: YT
authors.lastname: Wang
mesh_terms: D000368:Aged; D001249:Asthma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D016022:Case-Control Studies; D002681:China; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics; D007249:Inflammation; D015850:Interleukin-6 / Q000235:genetics*; D008175:Lung Neoplasms / Q000209:etiology / Q000235:genetics*; D008875:Middle Aged; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D012907:Smoking
chemical_list: D015850:Interleukin-6