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First genome-wide association study of esophageal atresia identifies three genetic risk loci at CTNNA3, FOXF1/FOXC2/FOXL1, and HNF1B
J. Gehlen, AS. Giel, R. Köllges, SL. Haas, R. Zhang, J. Trcka, AÖ. Sungur, F. Renziehausen, D. Bornholdt, D. Jung, PD. Hoyer, A. Nordenskjöld, D. Tibboel, J. Vlot, MCW. Spaander, R. Smigiel, D. Patkowski, N. Roeleveld, IA. van Rooij, I. de...
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 2020
PubMed Central
od 2020
ROAD: Directory of Open Access Scholarly Resources
od 2020
- Publikační typ
- časopisecké články MeSH
Esophageal atresia with or without tracheoesophageal fistula (EA/TEF) is the most common congenital malformation of the upper digestive tract. This study represents the first genome-wide association study (GWAS) to identify risk loci for EA/TEF. We used a European case-control sample comprising 764 EA/TEF patients and 5,778 controls and observed genome-wide significant associations at three loci. On chromosome 10q21 within the gene CTNNA3 (p = 2.11 × 10-8; odds ratio [OR] = 3.94; 95% confidence interval [CI], 3.10-5.00), on chromosome 16q24 next to the FOX gene cluster (p = 2.25 × 10-10; OR = 1.47; 95% CI, 1.38-1.55) and on chromosome 17q12 next to the gene HNF1B (p = 3.35 × 10-16; OR = 1.75; 95% CI, 1.64-1.87). We next carried out an esophageal/tracheal transcriptome profiling in rat embryos at four selected embryonic time points. Based on these data and on already published data, the implicated genes at all three GWAS loci are promising candidates for EA/TEF development. We also analyzed the genetic EA/TEF architecture beyond the single marker level, which revealed an estimated single-nucleotide polymorphism (SNP)-based heritability of around 37% ± 14% standard deviation. In addition, we examined the polygenicity of EA/TEF and found that EA/TEF is less polygenic than other complex genetic diseases. In conclusion, the results of our study contribute to a better understanding on the underlying genetic architecture of ET/TEF with the identification of three risk loci and candidate genes.
Center for Mind Brain and Behavior Philipps University Marburg Marburg Germany
Center of Pediatric Surgery Hannover Hannover Medical School Hannover Germany
Clinic for Neurology Section Neurobiological Research RWTH Aachen University Clinic Aachen Germany
Cologne Center for Genomics University of Cologne Cologne Germany
Department of Clinical Chemistry and Clinical Pharmacology University of Bonn Bonn Germany
Department of Clinical Genetics Erasmus Medical Centre Rotterdam the Netherlands
Department of Developmental Genetics Max Planck Institute for Molecular Genetics Berlin Germany
Department of Digestive Tract Diseases Medical University of Lodz Lodz Poland
Department of Genomics Life and Brain Center University of Bonn Bonn Germany
Department of Medical Epidemiology and Biostatistics Karolinska Institutet Stockholm Sweden
Department of Nutrition University of North Carolina at Chapel Hill Chapel Hill NC USA
Department of Paediatric Surgery Karolinska University Hospital Stockholm Sweden
Department of Pediatric Surgery and Urology Cnopf'sche Kinderklinik Nürnberg Germany
Department of Pediatric Surgery and Urology Medical University of Bialystok Poland
Department of Pediatric Surgery and Urology University Hospital Cologne Cologne Germany
Department of Pediatric Surgery and Urology Wroclaw Medical University Wroclaw Poland
Department of Pediatric Surgery Asklepios Children's Hospital St Augustin St Augustin Germany
Department of Pediatric Surgery Children's Hospital University of Tübingen Tübingen Germany
Department of Pediatric Surgery Ernst von Bergmann Hospital Potsdam Germany
Department of Pediatric Surgery Marien Hospital Witten Ruhr University Bochum Germany
Department of Pediatric Surgery Medical Center Dortmund Dortmund Germany
Department of Pediatric Surgery Skåne University Hospital Lund Sweden
Department of Pediatric Surgery University Children's Hospital Marburg Germany
Department of Pediatric Surgery University Hospital Bonn Bonn Germany
Department of Pediatric Surgery University Medical Center Hamburg Eppendorf Hamburg Germany
Department of Pediatric Surgery University Medicine Mainz Mainz Germany
Department of Pediatric Surgery University of Leipzig Leipzig Germany
Department of Pediatrics Children's Hospital University Hospital Bonn Bonn Germany
Department of Psychiatry University of North Carolina at Chapel Hill Chapel Hill NC USA
Department of Women's and Children's Health Karolinska Institutet Stockholm Sweden
Division of Cancer Biology and Genetics Queen's University Kingston Canada
Institute of Human Genetics University Hospital of Marburg Marburg Germany
Institute of Medical Biometry Informatics and Epidemiology University of Bonn Bonn Germany
KU Leuven Leuven Brain Institute Leuven Belgium
Perioperative Medicine and Intensive Care Karolinska University Stockholm Sweden
School of Medicine Faculty of Health University of Witten Herdecke Witten Germany
Citace poskytuje Crossref.org
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- $a First genome-wide association study of esophageal atresia identifies three genetic risk loci at CTNNA3, FOXF1/FOXC2/FOXL1, and HNF1B / $c J. Gehlen, AS. Giel, R. Köllges, SL. Haas, R. Zhang, J. Trcka, AÖ. Sungur, F. Renziehausen, D. Bornholdt, D. Jung, PD. Hoyer, A. Nordenskjöld, D. Tibboel, J. Vlot, MCW. Spaander, R. Smigiel, D. Patkowski, N. Roeleveld, IA. van Rooij, I. de Blaauw, A. Hölscher, M. Pauly, A. Leutner, J. Fuchs, J. Niethammer, MT. Melissari, E. Jenetzky, N. Zwink, H. Thiele, AC. Hilger, T. Hess, J. Trautmann, M. Marks, M. Baumgarten, G. Bläss, M. Landén, B. Fundin, CM. Bulik, T. Pennimpede, M. Ludwig, KU. Ludwig, E. Mangold, S. Heilmann-Heimbach, S. Moebus, BG. Herrmann, K. Alsabeah, CM. Burgos, HE. Lilja, S. Azodi, P. Stenström, E. Arnbjörnsson, B. Frybova, DM. Lebensztejn, W. Debek, E. Kolodziejczyk, K. Kozera, J. Kierkus, P. Kaliciński, M. Stefanowicz, A. Socha-Banasiak, M. Kolejwa, A. Piaseczna-Piotrowska, E. Czkwianianc, MM. Nöthen, P. Grote, M. Rygl, K. Reinshagen, N. Spychalski, B. Ludwikowski, J. Hubertus, A. Heydweiller, B. Ure, OJ. Muensterer, O. Aubert, JH. Gosemann, M. Lacher, P. Degenhardt, TM. Boemers, A. Mokrowiecka, E. Małecka-Panas, M. Wöhr, M. Knapp, G. Seitz, A. de Klein, G. Oracz, E. Brosens, H. Reutter, J. Schumacher
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- $a Esophageal atresia with or without tracheoesophageal fistula (EA/TEF) is the most common congenital malformation of the upper digestive tract. This study represents the first genome-wide association study (GWAS) to identify risk loci for EA/TEF. We used a European case-control sample comprising 764 EA/TEF patients and 5,778 controls and observed genome-wide significant associations at three loci. On chromosome 10q21 within the gene CTNNA3 (p = 2.11 × 10-8; odds ratio [OR] = 3.94; 95% confidence interval [CI], 3.10-5.00), on chromosome 16q24 next to the FOX gene cluster (p = 2.25 × 10-10; OR = 1.47; 95% CI, 1.38-1.55) and on chromosome 17q12 next to the gene HNF1B (p = 3.35 × 10-16; OR = 1.75; 95% CI, 1.64-1.87). We next carried out an esophageal/tracheal transcriptome profiling in rat embryos at four selected embryonic time points. Based on these data and on already published data, the implicated genes at all three GWAS loci are promising candidates for EA/TEF development. We also analyzed the genetic EA/TEF architecture beyond the single marker level, which revealed an estimated single-nucleotide polymorphism (SNP)-based heritability of around 37% ± 14% standard deviation. In addition, we examined the polygenicity of EA/TEF and found that EA/TEF is less polygenic than other complex genetic diseases. In conclusion, the results of our study contribute to a better understanding on the underlying genetic architecture of ET/TEF with the identification of three risk loci and candidate genes.
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