Genome-wide association scan of tag SNPs identifies a susceptibility locus for lung cancer at 15q25.1
Open accessAbstract
To identify risk variants for lung cancer, we conducted a multistage genome-wide association study. In the discovery phase, we analyzed 315,450 tagging SNPs in 1,154 current and former (ever) smoking cases of European ancestry and 1,137 frequency-matched, ever-smoking controls from Houston, Texas. For replication, we evaluated the ten SNPs most significantly associated with lung cancer in an additional 711 cases and 632 controls from Texas and 2,013 cases and 3,062 controls from the UK. Two SNPs, rs1051730 and rs8034191, mapping to a region of strong linkage disequilibrium within 15q25.1 containing PSMA4 and the nicotinic acetylcholine receptor subunit genes CHRNA3 and CHRNA5, were significantly associated with risk in both replication sets. Combined analysis yielded odds ratios of 1.32 (P < 1 x 10(-17)) for both SNPs. Haplotype analysis was consistent with there being a single risk variant in this region. We conclude that variation in a region of 15q25.1 containing nicotinic acetylcholine receptors genes contributes to lung cancer risk.
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Genetic variability in CHRNA5 is a major risk factor for lung cancer and COPD in smokers, likely reflecting higher tobacco dependence and greater exposure to carcinogens and toxins.
“In addition, the same genetic variability in CHRNA5 is also a major risk factor for lung cancer and chronic obstructive pulmonary disease (COPD) in smokers (Amos et al. 2008;Hung et al. 2008;Wang et al. 2010), likely reflecting higher levels of tobacco dependence in individuals carrying risk alleles and consequently greater exposure to carcinogens and”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Amos et al. 2008
The Abstract reports that variants in a region containing CHRNA5 are associated with lung cancer risk in ever-smokers. It does not establish CHRNA5 specifically as the causal gene or address COPD. Its smoking-behavior analysis found only weak evidence of an effect on dependence and says the lung-cancer association persisted after adjustment for smoking exposure, so it does not support the proposed explanation of greater carcinogen exposure. (LLM, conf=0.89)
Experimental — accuracy not yet measuredThe replicated nicotine dependence loci tagged by rs16969968 and rs578776 have also been reported to influence lung cancer risk in several genome-wide association studies.
“The replicated nicotine dependence loci tagged by rs16969968 (96,100–102) and rs578776 (101,103) have also been reported to influence lung cancer risk in several genome-wide association studies.”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [100]
Other reports indicate an increased risk of lung cancer even in nonsmokers, suggesting the possibility of a direct effect on lung cancer vulnerability.
“while others report an increased risk of lung cancer even in nonsmokers, suggesting the possibility of a direct effect on lung cancer vulnerability (101,104).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [104]
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- Authors
- Amos, C. I., Wu, X., Broderick, P., Gorlov, I. P., Gu, J., Eisen, T., Dong, Q., Zhang, Q., Gu, X., Vijayakrishnan, J., Sullivan, K., Matakidou, A., Wang, Y., Mills, G., Doheny, K., Tsai, Y.-Y., Chen, W. V., Shete, S., Spitz, M. R., & Houlston, R. S.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Institute of Cancer Research (GB)
- University of Cambridge (GB)
- Johns Hopkins University (US)
- Corresponding author
- Amos, Christopher I
- ORCID
- Venue
- Nature Genetics
- Published
- 2008-04-02
- Volume
- 40
- Issue
- 5
- Pages
- 616-622
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC2713680
- OpenAlex
- W1972020976
- Cited by
- 1,310
- References
- 24
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 19 · 2023: 42 · 2022: 33 · 2021: 30 · 2020: 89 · 2019: 43 · 2018: 37 · 2017: 61 · 2016: 58 · 2015: 97 · 2014: 89 · 2013: 94 · 2012: 131
- FWCI
- 85.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Johns Hopkins University
- Cancer Research UK
- National Institutes of Health (n01hg065403-000)
- National Human Genome Research Institute (N01 HG065403)
- National Cancer Institute (R01CA127219, R01 CA 55769, (P50-CA70907, R01CA133996, R01CA055769, P50CA070907, R01CA121197)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
- Keywords
- lung cancer, genetic susceptibility, nicotinic acetylcholine receptors, CHRNA3, CHRNA5, PSMA4, rs1051730, smoking, haplotype analysis, linkage disequilibrium, tag SNPs
- MeSH terms
- Aged, Chromosomes, Human, Pair 15, Cysteine Endopeptidases, Female, Genetic Testing, Haplotypes, Humans, Genetic Linkage, Lung Neoplasms, Male, Middle Aged, Nerve Tissue Proteins, Receptors, Nicotinic, Genome, Human, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide
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