Author
Listed:
- Jiyuan An
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
- Puya Gharahkhani
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
- Matthew H. Law
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
- Jue-Sheng Ong
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
- Xikun Han
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
- Catherine M. Olsen
(Cancer Control, QIMR Berghofer Medical Research Institute)
- Rachel E. Neale
(Cancer Aetiology and Prevention, QIMR Berghofer Medical Research Institute
The University of Queensland
the Queensland University of Technology)
- John Lai
(The University of Melbourne)
- Tom L. Vaughan
(Division of Public Health Sciences, Fred Hutchinson Cancer Research Center)
- Ines Gockel
(Thoracic and Vascular Surgery, University Hospital of Leipzig)
- René Thieme
(Thoracic and Vascular Surgery, University Hospital of Leipzig)
- Anne C. Böhmer
(University of Bonn, School of Medicine & University Hospital Bonn
University of Bonn)
- Janusz Jankowski
(Royal College of Surgeons in Ireland)
- Rebecca C. Fitzgerald
(Hutchison-MRC Research Centre and University of Cambridge)
- Johannes Schumacher
(University of Bonn, School of Medicine & University Hospital Bonn
University of Bonn
University Hospital of Marburg)
- Claire Palles
(University of Birmingham)
- David C. Whiteman
(Cancer Control, QIMR Berghofer Medical Research Institute)
- Stuart MacGregor
(Statistical Genetics, QIMR Berghofer Medical Research Institute)
Abstract
Gastroesophageal reflux disease (GERD) is caused by gastric acid entering the esophagus. GERD has high prevalence and is the major risk factor for Barrett’s esophagus (BE) and esophageal adenocarcinoma (EA). We conduct a large GERD GWAS meta-analysis (80,265 cases, 305,011 controls), identifying 25 independent genome-wide significant loci for GERD. Several of the implicated genes are existing or putative drug targets. Loci discovery is greatest with a broad GERD definition (including cases defined by self-report or medication data). Further, 91% of the GERD risk-increasing alleles also increase BE and/or EA risk, greatly expanding gene discovery for these traits. Our results map genes for GERD and related traits and uncover potential new drug targets for these conditions.
Suggested Citation
Jiyuan An & Puya Gharahkhani & Matthew H. Law & Jue-Sheng Ong & Xikun Han & Catherine M. Olsen & Rachel E. Neale & John Lai & Tom L. Vaughan & Ines Gockel & René Thieme & Anne C. Böhmer & Janusz Janko, 2019.
"Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases,"
Nature Communications, Nature, vol. 10(1), pages 1-10, December.
Handle:
RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11968-2
DOI: 10.1038/s41467-019-11968-2
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