Journal Article

Polymorphisms in inflammatory pathway genes, host factors and lung cancer risk in Chinese female never-smokers

Wei-Yen Lim, Ying Chen, Safiyya Mohamed Ali, Khoon Leong Chuah, Philip Eng, Swan Swan Leong, Elaine Lim, Tow Keang Lim, Alan WK Ng, Wee Teng Poh, Augustine Tee, Ming Teh, Agus Salim and Adeline Seow

in Carcinogenesis

Volume 32, issue 4, pages 522-529
Published in print April 2011 | ISSN: 0143-3334
Published online January 2011 | e-ISSN: 1460-2180 | DOI:
Polymorphisms in inflammatory pathway genes, host factors and lung cancer risk in Chinese female never-smokers

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  • Clinical Cytogenetics and Molecular Genetics


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Inflammation appears to be important in lung carcinogenesis among smokers, but its role among never-smokers is not well established. We hypothesized that inflammatory medical conditions and gene polymorphisms interact to increase lung cancer risk in never-smokers. We interviewed 433 Singaporean female never-smoker lung cancer patients and 1375 hospital controls, and evaluated six polymorphisms in the interleukin 1-β, interleukin 6 (IL6), cyclooxygenase-2, peroxisome proliferator-activated receptor-γ and interleukin 1-β receptor antagonist (IL1RN) genes. Tuberculosis was associated with a non-significant elevated risk of lung cancer [odds ratio (OR) 1.58, 95% confidence interval (CI) 0.95–2.62]. There was no effect of asthma, atopy or chronic productive cough individually. However, the presence of one or more of these conditions (asthma, cough or atopy) increased risk (OR 2.24, 95%CI 1.15–4.38) in individuals possessing the T/T genotype at interleukin 1-β -31T/C, but not in those possessing the C/T (OR 0.87, 95%CI 0.51–1.57) or C/C genotypes (OR 0.58, 95%CI 0.27–1.27), and in individuals having the *2 variable number of tandem repeat allele of IL1RN [OR 5.09 (1.39–18.67)], but not in those without (OR 0.93, 95%CI 0.63–1.35). The IL6-634 G allele increased the risk of lung cancer (OR 1.44, 95%CI 1.07–1.94). Lung cancer risk also increased with the number of polymorphism sites where at least 1 ‘risk’ allele was present [interleukin 1-β -31T/C (T allele), IL1RN (*2 allele) and IL6-634C/G (G allele)] among those with asthma, cough or atopy (Ptrend 0.001) but not in those without (Ptrend 0.47). Our results suggest that the effect of inflammatory medical conditions on lung cancer in never-smokers is modulated by host genetic susceptibility and will need to be confirmed in other studies conducted in similar populations.

Journal Article.  6489 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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