A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25

Where there's smoke... With the advent of large genomic data sets, geneticists can examine at a new level the influence of genes on behaviour. Two groups have conducted genome-wide association studies involving lung cancer, and both find that sequences in the nicotinic acetylcholine receptor su...

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Published inNature Vol. 452; no. 7187; pp. 633 - 637
Main Authors Hung, Rayjean J., McKay, James D., Gaborieau, Valerie, Boffetta, Paolo, Hashibe, Mia, Zaridze, David, Mukeria, Anush, Szeszenia-Dabrowska, Neonilia, Lissowska, Jolanta, Rudnai, Peter, Fabianova, Eleonora, Mates, Dana, Bencko, Vladimir, Foretova, Lenka, Janout, Vladimir, Chen, Chu, Goodman, Gary, Field, John K., Liloglou, Triantafillos, Xinarianos, George, Cassidy, Adrian, McLaughlin, John, Liu, Geoffrey, Narod, Steven, Krokan, Hans E., Skorpen, Frank, Elvestad, Maiken Bratt, Hveem, Kristian, Vatten, Lars, Linseisen, Jakob, Clavel-Chapelon, Françoise, Vineis, Paolo, Bueno-de-Mesquita, H. Bas, Lund, Eiliv, Martinez, Carmen, Bingham, Sheila, Rasmuson, Torgny, Hainaut, Pierre, Riboli, Elio, Ahrens, Wolfgang, Benhamou, Simone, Lagiou, Pagona, Trichopoulos, Dimitrios, Holcátová, Ivana, Merletti, Franco, Kjaerheim, Kristina, Agudo, Antonio, Macfarlane, Gary, Talamini, Renato, Simonato, Lorenzo, Lowry, Ray, Conway, David I., Znaor, Ariana, Healy, Claire, Zelenika, Diana, Boland, Anne, Delepine, Marc, Foglio, Mario, Lechner, Doris, Matsuda, Fumihiko, Blanche, Helene, Gut, Ivo, Heath, Simon, Lathrop, Mark, Brennan, Paul
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 03.04.2008
Nature Publishing Group
Subjects
Amino acids
Cancer
Carcinogens
Chromosomes, Human, Pair 15 - genetics
Europe
Genetic factors
Genetic Predisposition to Disease - genetics
Genomics
Genotype
Health risks
Humanities and Social Sciences
Humans
letter
Life Sciences
Lung cancer
Lung Neoplasms - genetics
multidisciplinary
Nicotine
Odds Ratio
Polymorphism, Single Nucleotide - genetics
Protein Subunits - genetics
Receptors, Nicotinic - genetics
Risk factors
Science
Science (multidisciplinary)
Smoking
Europe
Online AccessGet full text
ISSN0028-0836
1476-4687
1476-4687
1476-4679
DOI10.1038/nature06885

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Abstract Where there's smoke... With the advent of large genomic data sets, geneticists can examine at a new level the influence of genes on behaviour. Two groups have conducted genome-wide association studies involving lung cancer, and both find that sequences in the nicotinic acetylcholine receptor subunit gene cluster contribute susceptibility, although the groups took different paths to this result. Hung et al . suggest that this susceptibility is not related to smoking status or frequency, and show association with a specific amino acid change. Thorgeirsson et al . find that alleles present in a cluster of nicotinic acid receptor genes do not influence whether or not a person smokes, but do affect the number of cigarettes smoked per day, and are therefore also associated with risk of lung cancer and peripheral arterial disease. Either way, the possible potential of nicotinic acetylcholine receptors as drug targets is underlined. A genome-wide association study for lung cancer finds that genetic sequences in the nicotinic acetylcholine receptor subunit gene cluster contribute susceptibility. Interestingly, this susceptibility is not related to smoking status or frequency, and seems to come from a change in an amino acid in the receptor itself. Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually 1 . To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer ( P = 9 × 10 -10 ). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls ( P = 5 × 10 -20 overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits ( CHRNA5 , CHRNA3 and CHRNB4 ). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines 2 , 3 , and they bind to N ′-nitrosonornicotine and potential lung carcinogens 4 . A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets 5 .
AbstractList Where there's smoke... With the advent of large genomic data sets, geneticists can examine at a new level the influence of genes on behaviour. Two groups have conducted genome-wide association studies involving lung cancer, and both find that sequences in the nicotinic acetylcholine receptor subunit gene cluster contribute susceptibility, although the groups took different paths to this result. Hung et al . suggest that this susceptibility is not related to smoking status or frequency, and show association with a specific amino acid change. Thorgeirsson et al . find that alleles present in a cluster of nicotinic acid receptor genes do not influence whether or not a person smokes, but do affect the number of cigarettes smoked per day, and are therefore also associated with risk of lung cancer and peripheral arterial disease. Either way, the possible potential of nicotinic acetylcholine receptors as drug targets is underlined. A genome-wide association study for lung cancer finds that genetic sequences in the nicotinic acetylcholine receptor subunit gene cluster contribute susceptibility. Interestingly, this susceptibility is not related to smoking status or frequency, and seems to come from a change in an amino acid in the receptor itself. Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually 1 . To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer ( P = 9 × 10 -10 ). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls ( P = 5 × 10 -20 overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits ( CHRNA5 , CHRNA3 and CHRNB4 ). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines 2 , 3 , and they bind to N ′-nitrosonornicotine and potential lung carcinogens 4 . A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets 5 .
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 10-10). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 10-20 overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets. [PUBLICATION ABSTRACT]
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 times 10 super(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 times 10 super(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually1. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 × 10$^{-10}$). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 × 10$^{-20}$ overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N′-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets
Audience Academic
Author McLaughlin, John
Krokan, Hans E.
Vineis, Paolo
Bingham, Sheila
Chen, Chu
Matsuda, Fumihiko
Agudo, Antonio
Healy, Claire
Lagiou, Pagona
Janout, Vladimir
Boland, Anne
Hveem, Kristian
Foglio, Mario
Clavel-Chapelon, Françoise
Martinez, Carmen
Liloglou, Triantafillos
Gaborieau, Valerie
Mukeria, Anush
Lund, Eiliv
Vatten, Lars
Riboli, Elio
Simonato, Lorenzo
Benhamou, Simone
Mates, Dana
Fabianova, Eleonora
Conway, David I.
Bueno-de-Mesquita, H. Bas
Rasmuson, Torgny
Hainaut, Pierre
Delepine, Marc
McKay, James D.
Liu, Geoffrey
Lathrop, Mark
Macfarlane, Gary
Linseisen, Jakob
Field, John K.
Talamini, Renato
Kjaerheim, Kristina
Goodman, Gary
Zelenika, Diana
Skorpen, Frank
Xinarianos, George
Szeszenia-Dabrowska, Neonilia
Hashibe, Mia
Bencko, Vladimir
Lissowska, Jolanta
Trichopoulos, Dimitrios
Blanche, Helene
Elvestad, Maiken Bratt
Rudnai, Peter
Lowry, Ray
Merletti, Franco
Hung, Rayjean J.
Cassidy, Adrian
Zaridze, David
Ahrens, Wolfgang
Foretova, Lenka
Brennan, Paul
Gut, Ivo
Boffetta, Paolo
Holcátová, Ivana
Narod, Steven
Lechner, Doris
Heath, Simon
Znaor, Ariana
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  fullname: Lathrop, Mark
  organization: Centre National de Genotypage, Institut Genomique, Commissariat à l’énergie Atomique, Evry 91000, France , Fondation Jean Dausset-CEPH
– sequence: 65
  givenname: Paul
  surname: Brennan
  fullname: Brennan, Paul
  email: brennan@iarc.fr
  organization: International Agency for Research on Cancer (IARC)
BackLink https://www.ncbi.nlm.nih.gov/pubmed/18385738$$D View this record in MEDLINE/PubMed
https://cea.hal.science/cea-00944415$$DView record in HAL
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-46004$$DView record from Swedish Publication Index
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Snippet Where there's smoke... With the advent of large genomic data sets, geneticists can examine at a new level the influence of genes on behaviour. Two groups have...
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we...
Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually1. To identify genetic factors that modify disease risk, we...
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StartPage 633
SubjectTerms Amino acids
Cancer
Carcinogens
Chromosomes, Human, Pair 15 - genetics
Europe
Genetic factors
Genetic Predisposition to Disease - genetics
Genomics
Genotype
Health risks
Humanities and Social Sciences
Humans
letter
Life Sciences
Lung cancer
Lung Neoplasms - genetics
multidisciplinary
Nicotine
Odds Ratio
Polymorphism, Single Nucleotide - genetics
Protein Subunits - genetics
Receptors, Nicotinic - genetics
Risk factors
Science
Science (multidisciplinary)
Smoking
Title A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25
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