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Large Scale Association Analysis Identifies Three Susceptibility Loci for Coronary Artery Disease (9p21 Is Associated with Coronary Artery Disease)

Genome wide association studies (GWAS) and their replications that have associated DNA variants with myocardial infarction (MI) and/or coronary artery disease (CAD) are predominantly based on populations of European or Eastern Asian descent. Replication of the most significantly associated polymorph... Full description

Journal Title: PLoS ONE 2011, Vol.6(12), p.e29427
Main Author: Saade, Stephanie
Other Authors: Cazier, Jean-Baptiste , Ghassibe-Sabbagh, Michella , Youhanna, Sonia , Badro, Danielle A , Kamatani, Yoichiro , Hager, Jörg , Yeretzian, Joumana S , El-Khazen, Georges , Haber, Marc , Salloum, Angelique K , Douaihy, Bouchra , Othman, Raed , Shasha, Nabil , Kabbani, Samer , Bayeh, Hamid El , Chammas, Elie , Farrall, Martin , Gauguier, Dominique , Platt, Daniel E , Zalloua, Pierre A
Format: Electronic Article Electronic Article
Language: English
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ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0029427
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recordid: plos10.1371/journal.pone.0029427
title: Large Scale Association Analysis Identifies Three Susceptibility Loci for Coronary Artery Disease (9p21 Is Associated with Coronary Artery Disease)
format: Article
creator:
  • Saade, Stephanie
  • Cazier, Jean-Baptiste
  • Ghassibe-Sabbagh, Michella
  • Youhanna, Sonia
  • Badro, Danielle A
  • Kamatani, Yoichiro
  • Hager, Jörg
  • Yeretzian, Joumana S
  • El-Khazen, Georges
  • Haber, Marc
  • Salloum, Angelique K
  • Douaihy, Bouchra
  • Othman, Raed
  • Shasha, Nabil
  • Kabbani, Samer
  • Bayeh, Hamid El
  • Chammas, Elie
  • Farrall, Martin
  • Gauguier, Dominique
  • Platt, Daniel E
  • Zalloua, Pierre A
subjects:
  • Research Article
  • Biology
  • Medicine
  • Genetics And Genomics
ispartof: PLoS ONE, 2011, Vol.6(12), p.e29427
description: Genome wide association studies (GWAS) and their replications that have associated DNA variants with myocardial infarction (MI) and/or coronary artery disease (CAD) are predominantly based on populations of European or Eastern Asian descent. Replication of the most significantly associated polymorphisms in multiple populations with distinctive genetic backgrounds and lifestyles is crucial to the understanding of the pathophysiology of a multifactorial disease like CAD. We have used our Lebanese cohort to perform a replication study of nine previously identified CAD/MI susceptibility loci ( LTA , CDKN2A - CDKN2B , CELSR2 - PSRC1 - SORT1 , CXCL12 , MTHFD1L , WDR12 , PCSK9 , SH2B3 , and SLC22A3 ), and 88 genes in related phenotypes. The study was conducted on 2,002 patients with detailed demographic, clinical characteristics, and cardiac catheterization results. One marker, rs6922269 , in MTHFD1L was significantly protective against MI (OR = 0.68, p = 0.0035), while the variant rs4977574 in CDKN2A - CDKN2B was significantly associated with MI (OR = 1.33, p = 0.0086). Associations were detected after adjustment for family history of CAD, gender, hypertension, hyperlipidemia, diabetes, and smoking. The parallel study of 88 previously published genes in related phenotypes encompassed 20,225 markers, three quarters of which with imputed genotypes The study was based on our genome-wide genotype data set, with imputation across the whole genome to HapMap II release 22 using HapMap CEU population as a reference. Analysis was conducted on both the genotyped and imputed variants in the 88 regions covering selected genes. This approach replicated HNRNPA3P1 - CXCL12 association with CAD and identified new significant associations of CDKAL1, ST6GAL1, and PTPRD with CAD. Our study provides evidence for the importance of the multifactorial aspect of CAD/MI and describes genes predisposing to their etiology.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0029427
fulltext: fulltext
issn:
  • 1932-6203
  • 19326203
url: Link


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titleLarge Scale Association Analysis Identifies Three Susceptibility Loci for Coronary Artery Disease (9p21 Is Associated with Coronary Artery Disease)
creatorSaade, Stephanie ; Cazier, Jean-Baptiste ; Ghassibe-Sabbagh, Michella ; Youhanna, Sonia ; Badro, Danielle A ; Kamatani, Yoichiro ; Hager, Jörg ; Yeretzian, Joumana S ; El-Khazen, Georges ; Haber, Marc ; Salloum, Angelique K ; Douaihy, Bouchra ; Othman, Raed ; Shasha, Nabil ; Kabbani, Samer ; Bayeh, Hamid El ; Chammas, Elie ; Farrall, Martin ; Gauguier, Dominique ; Platt, Daniel E ; Zalloua, Pierre A
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0029427
subjectResearch Article ; Biology ; Medicine ; Genetics And Genomics
descriptionGenome wide association studies (GWAS) and their replications that have associated DNA variants with myocardial infarction (MI) and/or coronary artery disease (CAD) are predominantly based on populations of European or Eastern Asian descent. Replication of the most significantly associated polymorphisms in multiple populations with distinctive genetic backgrounds and lifestyles is crucial to the understanding of the pathophysiology of a multifactorial disease like CAD. We have used our Lebanese cohort to perform a replication study of nine previously identified CAD/MI susceptibility loci ( LTA , CDKN2A - CDKN2B , CELSR2 - PSRC1 - SORT1 , CXCL12 , MTHFD1L , WDR12 , PCSK9 , SH2B3 , and SLC22A3 ), and 88 genes in related phenotypes. The study was conducted on 2,002 patients with detailed demographic, clinical characteristics, and cardiac catheterization results. One marker, rs6922269 , in MTHFD1L was significantly protective against MI (OR = 0.68, p = 0.0035), while the variant rs4977574 in CDKN2A - CDKN2B was significantly associated with MI (OR = 1.33, p = 0.0086). Associations were detected after adjustment for family history of CAD, gender, hypertension, hyperlipidemia, diabetes, and smoking. The parallel study of 88 previously published genes in related phenotypes encompassed 20,225 markers, three quarters of which with imputed genotypes The study was based on our genome-wide genotype data set, with imputation across the whole genome to HapMap II release 22 using HapMap CEU population as a reference. Analysis was conducted on both the genotyped and imputed variants in the 88 regions covering selected genes. This approach replicated HNRNPA3P1 - CXCL12 association with CAD and identified new significant associations of CDKAL1, ST6GAL1, and PTPRD with CAD. Our study provides evidence for the importance of the multifactorial aspect of CAD/MI and describes genes predisposing to their etiology.
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descriptionGenome wide association studies (GWAS) and their replications that have associated DNA variants with myocardial infarction (MI) and/or coronary artery disease (CAD) are predominantly based on populations of European or Eastern Asian descent. Replication of the most significantly associated polymorphisms in multiple populations with distinctive genetic backgrounds and lifestyles is crucial to the understanding of the pathophysiology of a multifactorial disease like CAD. We have used our Lebanese cohort to perform a replication study of nine previously identified CAD/MI susceptibility loci ( LTA , CDKN2A - CDKN2B , CELSR2 - PSRC1 - SORT1 , CXCL12 , MTHFD1L , WDR12 , PCSK9 , SH2B3 , and SLC22A3 ), and 88 genes in related phenotypes. The study was conducted on 2,002 patients with detailed demographic, clinical characteristics, and cardiac catheterization results. One marker, rs6922269 , in MTHFD1L was significantly protective against MI (OR = 0.68, p = 0.0035), while the variant rs4977574 in CDKN2A - CDKN2B was significantly associated with MI (OR = 1.33, p = 0.0086). Associations were detected after adjustment for family history of CAD, gender, hypertension, hyperlipidemia, diabetes, and smoking. The parallel study of 88 previously published genes in related phenotypes encompassed 20,225 markers, three quarters of which with imputed genotypes The study was based on our genome-wide genotype data set, with imputation across the whole genome to HapMap II release 22 using HapMap CEU population as a reference. Analysis was conducted on both the genotyped and imputed variants in the 88 regions covering selected genes. This approach replicated HNRNPA3P1 - CXCL12 association with CAD and identified new significant associations of CDKAL1, ST6GAL1, and PTPRD with CAD. Our study provides evidence for the importance of the multifactorial aspect of CAD/MI and describes genes predisposing to their etiology.
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abstractGenome wide association studies (GWAS) and their replications that have associated DNA variants with myocardial infarction (MI) and/or coronary artery disease (CAD) are predominantly based on populations of European or Eastern Asian descent. Replication of the most significantly associated polymorphisms in multiple populations with distinctive genetic backgrounds and lifestyles is crucial to the understanding of the pathophysiology of a multifactorial disease like CAD. We have used our Lebanese cohort to perform a replication study of nine previously identified CAD/MI susceptibility loci ( LTA , CDKN2A - CDKN2B , CELSR2 - PSRC1 - SORT1 , CXCL12 , MTHFD1L , WDR12 , PCSK9 , SH2B3 , and SLC22A3 ), and 88 genes in related phenotypes. The study was conducted on 2,002 patients with detailed demographic, clinical characteristics, and cardiac catheterization results. One marker, rs6922269 , in MTHFD1L was significantly protective against MI (OR = 0.68, p = 0.0035), while the variant rs4977574 in CDKN2A - CDKN2B was significantly associated with MI (OR = 1.33, p = 0.0086). Associations were detected after adjustment for family history of CAD, gender, hypertension, hyperlipidemia, diabetes, and smoking. The parallel study of 88 previously published genes in related phenotypes encompassed 20,225 markers, three quarters of which with imputed genotypes The study was based on our genome-wide genotype data set, with imputation across the whole genome to HapMap II release 22 using HapMap CEU population as a reference. Analysis was conducted on both the genotyped and imputed variants in the 88 regions covering selected genes. This approach replicated HNRNPA3P1 - CXCL12 association with CAD and identified new significant associations of CDKAL1, ST6GAL1, and PTPRD with CAD. Our study provides evidence for the importance of the multifactorial aspect of CAD/MI and describes genes predisposing to their etiology.
copSan Francisco, USA
pubPublic Library of Science
doi10.1371/journal.pone.0029427
oafree_for_read
date2011-12-27