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Association Analyses Identify 38 Susceptibility Loci for Inflammatory Bowel Disease and Highlight Shared Genetic Risk Across Populations Publisher Pubmed



Liu JZ1 ; Van Sommeren S2, 3 ; Huang H4 ; Ng SC5 ; Alberts R2 ; Takahashi A6 ; Ripke S4 ; Lee JC7 ; Jostins L8 ; Shah T1 ; Abedian S9 ; Cheon JH10 ; Cho J11 ; Daryani NE12 Show All Authors
Authors
  1. Liu JZ1
  2. Van Sommeren S2, 3
  3. Huang H4
  4. Ng SC5
  5. Alberts R2
  6. Takahashi A6
  7. Ripke S4
  8. Lee JC7
  9. Jostins L8
  10. Shah T1
  11. Abedian S9
  12. Cheon JH10
  13. Cho J11
  14. Daryani NE12
  15. Franke L3
  16. Fuyuno Y13
  17. Hart A14
  18. Juyal RC15
  19. Juyal G16
  20. Kim WH10
  21. Morris AP17
  22. Poustchi H9
  23. Newman WG18
  24. Midha V19
  25. Orchard TR20
  26. Vahedi H9
  27. Sood A19
  28. Sung JJY5
  29. Malekzadeh R9
  30. Westra HJ3
  31. Yamazaki K13
  32. Yang SK21
  33. Barrett JC1
  34. Franke A22
  35. Alizadeh BZ23
  36. Parkes M7
  37. Thelma BK16
  38. Daly MJ4
  39. Kubo M13
  40. Anderson CA1
  41. Weersma RK2
Show Affiliations
Authors Affiliations
  1. 1. Wellcome Trust Sanger Institute, Hinxton, United Kingdom
  2. 2. Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands
  3. 3. Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, Netherlands
  4. 4. Analytic and Translational Genetics Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States
  5. 5. Department of Medicine and Therapeutics, Institute of Digestive Disease, LKS Institute of Health Science, State Key Laboratory of Digestive Disease, Chinese University of Hong Kong, Hong Kong
  6. 6. Laboratory for Statistical Analysis, Center for Integrative Medical Sciences, RIKEN, Yokohama, Japan
  7. 7. Inflammatory Bowel Disease Research Group, Addenbrooke's Hospital, Cambridge, United Kingdom
  8. 8. Wellcome Trust Centre for Human Genetics, University of Oxford, Headington, United Kingdom
  9. 9. Digestive Disease Research Institute, Shariati Hospital, Tehran, Iran
  10. 10. Department of Gastroenterology and Hepatology, Yonsei University College of Medicine, Seoul, South Korea
  11. 11. Icahn School of Medicine, Mount Sinai Hospital, New York, NY, United States
  12. 12. Department of Gastroenterology, Emam Hospital, Tehran, Iran
  13. 13. Laboratory for Genotyping Development, Center for Integrative Medical Sciences, RIKEN, Yokohama, Japan
  14. 14. Inflammatory Bowel Disease Unit, St Mark's Hospital, Harrow, United Kingdom
  15. 15. National Institute of Immunology, New Delhi, India
  16. 16. Department of Genetics, University of Delhi South Campus, New Delhi, India
  17. 17. Department of Biostatistics, University of Liverpool, Liverpool, United Kingdom
  18. 18. Manchester Centre for Genomic Medicine, University of Manchester, Central Manchester University Hospitals National Health Service (NHS) Foundation Trust, Manchester, United Kingdom
  19. 19. Department of Medicine, Dayanand Medical College and Hospital, Ludhiana, India
  20. 20. Department of Gastroenterology and Hepatology, St. Mary's Hospital, London, United Kingdom
  21. 21. Department of Gastroenterology and Hepatology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea
  22. 22. Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany
  23. 23. Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands

Source: Nature Genetics Published:2015


Abstract

Ulcerative colitis and Crohn's disease are the two main forms of inflammatory bowel disease (IBD). Here we report the first trans-ancestry association study of IBD, with genome-wide or Immunochip genotype data from an extended cohort of 86,640 European individuals and Immunochip data from 9,846 individuals of East Asian, Indian or Iranian descent. We implicate 38 loci in IBD risk for the first time. For the majority of the IBD risk loci, the direction and magnitude of effect are consistent in European and non-European cohorts. Nevertheless, we observe genetic heterogeneity between divergent populations at several established risk loci driven by differences in allele frequency (NOD2) or effect size (TNFSF15 and ATG16L1) or a combination of these factors (IL23R and IRGM). Our results provide biological insights into the pathogenesis of IBD and demonstrate the usefulness of trans-ancestry association studies for mapping loci associated with complex diseases and understanding genetic architecture across diverse populations. © 2015 Nature America, Inc. All rights reserved.
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