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Eur J Hum Genet. 2015 Dec;23(12):1723-8. doi: 10.1038/ejhg.2015.48. Epub 2015 Mar 25.

Deciphering associations for lung cancer risk through imputation and analysis of 12,316 cases and 16,831 controls.

Author information

1
Division of Genetics and Epidemiology, The Institute of Cancer Research, Surrey, Sutton, UK.
2
Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.
3
International Agency for Research on Cancer (IARC, World Health Organization (WHO)), Lyon, France.
4
Division of Cancer Epidemiology and Genetics, National Cancer institute, NIH, DHHS, Bethesda, MD, USA.
5
Department of Community and Family Medicine, Geisel School of Medicine, Center for Genomic Medicine, Lebanon, NH, USA.
6
Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK.
7
Addenbrooke's Hospital, Cambridge Biomedical Campus, Cambridge, UK.
8
Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD, USA.

Abstract

Recent genome-wide association studies have identified common variants at multiple loci influencing lung cancer risk. To decipher the genetic basis of the association signals at 3q28, 5p15.33, 6p21.33, 9p21 and 12p13.33, we performed a meta-analysis of data from five genome-wide association studies in populations of European ancestry totalling 12 316 lung cancer cases and 16 831 controls using imputation to recover untyped genotypes. For four of the regions, it was possible to refine the association signal identifying a smaller region of interest likely to harbour the functional variant. Our analysis did not provide evidence that any of the associations at the loci being a consequence of synthetic associations rather than linkage disequilibrium with a common risk variant at these risk loci.

PMID:
25804397
PMCID:
PMC4795209
DOI:
10.1038/ejhg.2015.48
[Indexed for MEDLINE]
Free PMC Article

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