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GWAS Study

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

An J, Gharahkhani P, Law MH et al.

31527586 PubMed ID
GWAS Study Type
32925 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

AJ
An J
GP
Gharahkhani P
LM
Law MH
OJ
Ong JS
HX
Han X
OC
Olsen CM
NR
Neale RE
LJ
Lai J
VT
Vaughan TL
GI
Gockel I
TR
Thieme R
BA
Böhmer AC
JJ
Jankowski J
FR
Fitzgerald RC
SJ
Schumacher J
PC
Palles C
WD
Whiteman DC
MS
MacGregor S
Chapter II

Abstract

Summary of the research findings

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.

8,998 European and unknown ancestry Barrett's esophagus cases, 4,680 European and unknown ancestry esophageal adenocarcinoma cases, 19,247 European and unknown ancestry controls

Chapter III

Study Statistics

Key metrics and study information

32925
Total Participants
GWAS
Study Type
No
Replicated
European, NR
Ancestry
Germany, U.K., Australia
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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