EconPapers    
Economics at your fingertips  
 

Gastroesophageal reflux GWAS identifies risk loci that also associate with subsequent severe esophageal diseases

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 Jankowski, Rebecca C. Fitzgerald, Johannes Schumacher, Claire Palles, David C. Whiteman and Stuart MacGregor ()
Additional contact information
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
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
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
Claire Palles: University of Birmingham
David C. Whiteman: Cancer Control, QIMR Berghofer Medical Research Institute
Stuart MacGregor: Statistical Genetics, QIMR Berghofer Medical Research Institute

Nature Communications, 2019, vol. 10, issue 1, 1-10

Abstract: 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.

Date: 2019
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-019-11968-2 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11968-2

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-019-11968-2

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().

 
Page updated 2025-03-19
Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11968-2