Abstract:
:Impaired lung function is often caused by cigarette smoking, making it challenging to disentangle its role in lung cancer susceptibility. Investigation of the shared genetic basis of these phenotypes in the UK Biobank and International Lung Cancer Consortium (29,266 cases, 56,450 controls) shows that lung cancer is genetically correlated with reduced forced expiratory volume in one second (FEV1: rg = 0.098, p = 2.3 × 10-8) and the ratio of FEV1 to forced vital capacity (FEV1/FVC: rg = 0.137, p = 2.0 × 10-12). Mendelian randomization analyses demonstrate that reduced FEV1 increases squamous cell carcinoma risk (odds ratio (OR) = 1.51, 95% confidence intervals: 1.21-1.88), while reduced FEV1/FVC increases the risk of adenocarcinoma (OR = 1.17, 1.01-1.35) and lung cancer in never smokers (OR = 1.56, 1.05-2.30). These findings support a causal role of pulmonary impairment in lung cancer etiology. Integrative analyses reveal that pulmonary function instruments, including 73 novel variants, influence lung tissue gene expression and implicate immune-related pathways in mediating the observed effects on lung carcinogenesis.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Kachuri L,Johansson M,Rashkin SR,Graff RE,Bossé Y,Manem V,Caporaso NE,Landi MT,Christiani DC,Vineis P,Liu G,Scelo G,Zaridze D,Shete SS,Albanes D,Aldrich MC,Tardón A,Rennert G,Chen C,Goodman GE,Doherty JA,Bickebödoi
10.1038/s41467-019-13855-2subject
Has Abstractpub_date
2020-01-07 00:00:00pages
27issue
1issn
2041-1723pii
10.1038/s41467-019-13855-2journal_volume
11pub_type
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