Journal
NATURE COMMUNICATIONS
Volume 10, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-11968-2
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Funding
- US National Cancer Institute at the National Institutes of Health [R01CA136725]
- National Health and Medical Research Council (NHMRC) Fellowships
- Australian NHMRC [APP1063061]
- National Cancer Institute
- Swedish Cancer Society [4559-B01-01XAA, 4758-B02-01XAB]
- US NIH [R01DK63616, R01CA59636]
- California Tobacco Related Research Program [3RT-0122, 10RT-0251]
- University of Texas MD Anderson Cancer Center (UTMDACC)
- NIH [R01CA100264, P30CA016672, R01CA133996]
- UTMDACC NIH SPORE in Melanoma [2P50CA093459]
- Marit Peterson Fund for Melanoma Research [HHSN268200782096C]
- Wellcome Trust medical charity, Medical Research Council (UK), Department of Health (UK)
- Scottish Government
- Northwest Regional Development Agency
- Welsh Assembly Government
- British Heart Foundation
- Diabetes UK
- Swedish Esophageal Cancer [R01 CA57947-03]
- Center for Inherited Disease Research (CIDR)
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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.
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