Genetic Association and Risk Scores in a Chronic Obstructive Pulmonary Disease Meta-analysis of 16,707 Subjects
The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine...
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Published in | American journal of respiratory cell and molecular biology Vol. 57; no. 1; pp. 35 - 46 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Thoracic Society
01.07.2017
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Subjects | |
Online Access | Get full text |
ISSN | 1044-1549 1535-4989 |
DOI | 10.1165/rcmb.2016-0331OC |
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Abstract | The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 × 10
) and PPP4R4/SERPINA1 (P = 1.01 × 10
) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function. |
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AbstractList | The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 × 10
) and PPP4R4/SERPINA1 (P = 1.01 × 10
) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function. The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P =1.28 X 1028) and PPP4R4/SERPINA1 (P = 1.01 X 10~8) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ~0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function. The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 × 10-8) and PPP4R4/SERPINA1 (P = 1.01 × 10-8) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function. The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: ( 1 ) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and ( 2 ) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC ( P = 1.28 × 10 −8 ) and PPP4R4/SERPINA1 ( P = 1.01 × 10 −8 ) and severe COPD; the latter association may be driven by recognized variants in SERPINA1 . Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9–1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1 . A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function. |
Author | Lutz, Sharon Castaldi, Peter Lomas, David A. Curtis, Jeffrey L. Beaty, Terri Stoel, Berend C. Calverley, Peter M. Kim, Deog K. Beaty, Terri H. Gray, Teresa Levy, Robert D. Cho, Michael H. Sieren, Jered Everett, Douglas Young, Kendra Hersh, Craig Martinez, Carlos H. Alapat, Philip Hobbs, Brian D. Busch, Robert Tschirren, Juerg El-Bouiez, Adel Silverman, Edwin K. Pernicano, Perry G. Parker, Margaret Hokanson, John E. Judy, Philip F. Kluiber, Alex Castaldi, Peter J. Donner, Claudio F. Silverman, Edwin Won, Sungho Paré, Peter D. San Jose Estepar, Raul Hobbs, Brian Han, MeiLan K. Coxson, Harvey O. Hansel, Nadia Wilson, Carla G. Bandi, Venkata Wan, Emily Rennard, Stephen I. Santorico, Stephanie DeMeo, Dawn Hokanson, John Litonjua, Augusto A. Duca, Lindsey Schroeder, Joyce Bakke, Per Hanania, Nicola Lange, Christoph McDonald, Merry-Lynn Newell, John D. McGeachie, Michael J. Agusti, Alvar Laird, Nan Kinney, Gregory Mann, Tanya Pratte, Katherine Hardin, Megan Washko, George Make, Barry Yim, Jae-Joon Vestbo, Jørgen Hoffman, Eric A. Van Beek, Edwin Hardin, Mega |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28170284$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Contributor | Washington, Lacey Schroeder, Joyce Lutz, Sharon Castaldi, Peter Rozenshtein, Anna Wise, Robert Beaty, Terri Casaburi, Richard Ross, James C Lynch, David A Hanania, Nicola Newell, Jr, John D MacIntyre, Jr, Neil Lange, Christoph Gray, Teresa Atik, Mustafa Pernicano, Perry G McDonald, Merry-Lynn Putcha, Nirupama Laird, Nan Kinney, Gregory Curtis, Jeffrey L Mann, Tanya Adami, Alessandra Sieren, Jered Everett, Douglas Young, Kendra Hersh, Craig Judy, Philip F Pratte, Katherine Hardin, Megan Washko, George Make, Barry Van Beek, Edwin Martinez, Carlos H Alapat, Philip Qiao, Dandi Kazerooni, Ella A D'Souza, Belinda Stinson, Douglas Busch, Robert Tschirren, Juerg El-Bouiez, Adel Rikxoort, Eva van Horton, Karen Parker, Margaret Stoel, Berend C Strand, Matt Hokanson, John E Wilson, Carla Barr, R Graham Han, MeiLan K Hetmanski, Jacqueline Kluiber, Alex Guy, Elizabeth Pearson, Gregory D N Boriek, Aladin Begum, Ferdouse Silverman, Edwin Won, Sungho Jacobson, Francine L Guntupalli, Kalpatha Al Qaisi, Mustafa San Jose Estepar, Raul Faino, Anna Parulekar, Amit Humphr |
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Copyright | Copyright American Thoracic Society Jul 2017 Copyright © 2017 by the American Thoracic Society 2017 |
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SubjectTerms | Aged Association analysis Chronic obstructive pulmonary disease Female Genetic diversity Genetic Predisposition to Disease Genetics Genome-Wide Association Study Genomes Genotyping Health risk assessment Heritability Humans Lung diseases Male Meta-analysis Middle Aged Obstructive lung disease Original Research Pulmonary Disease, Chronic Obstructive - diagnosis Pulmonary Disease, Chronic Obstructive - genetics Pulmonary Disease, Chronic Obstructive - physiopathology Respiratory function Respiratory Function Tests Risk Factors Single-nucleotide polymorphism Smoking Studies |
Title | Genetic Association and Risk Scores in a Chronic Obstructive Pulmonary Disease Meta-analysis of 16,707 Subjects |
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