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Carcinogenesis Advance Access originally published online on December 12, 2005
Carcinogenesis 2006 27(6):1240-1244; doi:10.1093/carcin/bgi309
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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

Adeline Seow 1, 3, *, Daniel PK Ng 1, 3, Serena Choo 3, Philip Eng 4, Wee-Teng Poh 5, Teh Ming 2 and Yee-Tang Wang 6

1 Department of Community, Occupational and Family Medicine, 2 Department of Pathology and 3 Centre for Molecular Epidemiology, National University of Singapore, Singapore, 4 Respiratory and Critical Care Medicine, Singapore General Hospital, Singapore, 5 Laboratory Medicine, Changi General Hospital, Singapore and 6 Respiratory Medicine, Tan Tock Seng Hospital, Singapore

* To whom correspondence should be addressed at: Department of Community, Occupational and Family Medicine, National University of Singapore, 16 Medical Drive, MD3, Singapore. Tel: +65 65164974; Fax: +65 67791489; E-mail: cofseowa{at}nus.edu.sg

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.


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