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 inAmerican journal of respiratory cell and molecular biology Vol. 57; no. 1; pp. 35 - 46
Main Authors Busch, Robert, Hobbs, Brian D., Zhou, Jin, Castaldi, Peter J., McGeachie, Michael J., Hardin, Megan E., Hawrylkiewicz, Iwona, Sliwinski, Pawel, Yim, Jae-Joon, Kim, Woo Jin, Kim, Deog K., Agusti, Alvar, Make, Barry J., Crapo, James D., Calverley, Peter M., Donner, Claudio F., Lomas, David A., Wouters, Emiel F., Vestbo, Jørgen, Tal-Singer, Ruth, Bakke, Per, Gulsvik, Amund, Litonjua, Augusto A., Sparrow, David, Paré, Peter D., Levy, Robert D., Rennard, Stephen I., Beaty, Terri H., Hokanson, John, Silverman, Edwin K., Cho, Michael H., Crapo, James, Silverman, Edwin, Make, Barry, Regan, Elizabeth, Beaty, Terri, Laird, Nan, Lange, Christoph, Cho, Michael, Santorico, Stephanie, DeMeo, Dawn, Hansel, Nadia, Hersh, Craig, Castaldi, Peter, McDonald, Merry-Lynn, Wan, Emily, Hardin, Megan, Hetmanski, Jacqueline, Parker, Margaret, Foreman, Marilyn, Hobbs, Brian, El-Bouiez, Adel, Qiao, Dandi, Halper-Stromberg, Eitan, Begum, Ferdouse, Won, Sungho, Lutz, Sharon, Lynch, David A., Coxson, Harvey O., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Newell, John D., Ross, James C., San Jose Estepar, Raul, Stoel, Berend C., Tschirren, Juerg, Rikxoort, Eva van, Ginneken, Bram van, Washko, George, Wilson, Carla G., Al Qaisi, Mustafa, Gray, Teresa, Kluiber, Alex, Mann, Tanya, Sieren, Jered, Stinson, Douglas, Schroeder, Joyce, Van Beek, Edwin, Jensen, Robert, Everett, Douglas, Faino, Anna, Strand, Matt, Wilson, Carla, Hokanson, John E., Kinney, Gregory, Young, Kendra, Pratte, Katherine, Duca, Lindsey, Curtis, Jeffrey L., Martinez, Carlos H., Pernicano, Perry G., Hanania, Nicola, Alapat, Philip, Bandi, Venkata
Format Journal Article
LanguageEnglish
Published United States American Thoracic Society 01.07.2017
Subjects
Online AccessGet full text
ISSN1044-1549
1535-4989
DOI10.1165/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.
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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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
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Copyright Copyright American Thoracic Society Jul 2017
Copyright © 2017 by the American Thoracic Society 2017
Copyright_xml – notice: Copyright American Thoracic Society Jul 2017
– notice: Copyright © 2017 by the American Thoracic Society 2017
CorporateAuthor International COPD Genetics Network
Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-Points
COPDGene Investigators
National Emphysema Treatment Trial Genetics
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Issue 1
Keywords alpha-1 antitrypsin
genetic risk score
genetic risk factors
chronic obstructive pulmonary disease
genetic epidemiology
Language English
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A full list of investigators is included before the References.
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PublicationTitle American journal of respiratory cell and molecular biology
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PublicationYear 2017
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Snippet The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving...
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StartPage 35
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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