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Cancer Epidemiol Biomarkers Prev. 2015 Nov;24(11):1801-3. doi: 10.1158/1055-9965.EPI-15-0596. Epub 2015 Sep 12.

Pleiotropic analysis of cancer risk loci on esophageal adenocarcinoma risk.

Author information

1
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California. leee@usc.edu.
2
Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
3
Statistical Genetics, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
4
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
5
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
6
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Division of Cancer Studies, King's College London, London, United Kingdom.
7
Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, University of North Carolina, Chapel Hill, North Carolina.
8
Centre for Public Health, Queen's University Belfast, United Kingdom.
9
Division of Epidemiology, University of Leeds, Leeds, United Kingdom.
10
Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina.
11
Department of Epidemiology, MD Anderson Cancer Center, Houston, Texas.
12
Yale School of Public Health, Department of Chronic Disease Epidemiology, New Haven, Connecticut.
13
Division of Research, Kaiser Permanente Northern California, Oakland, California. San Francisco Medical Center, Kaiser Permanente Northern California, San Francisco, California.
14
Department of Biostatistics, University of Washington School of Public Health, Seattle, Washington.
15
Cancer Control, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
16
Department of Population Sciences, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Duarte, California.
17
Department of Oncology, University of Sheffield Medical School, Sheffield, United Kingdom.

Abstract

BACKGROUND:

Several cancer-associated loci identified from genome-wide association studies (GWAS) have been associated with risks of multiple cancer sites, suggesting pleiotropic effects. We investigated whether GWAS-identified risk variants for other common cancers are associated with risk of esophageal adenocarcinoma (EA) or its precursor, Barrett's esophagus.

METHODS:

We examined the associations between risks of EA and Barrett's esophagus and 387 SNPs that have been associated with risks of other cancers, by using genotype imputation data on 2,163 control participants and 3,885 (1,501 EA and 2,384 Barrett's esophagus) case patients from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study, and investigated effect modification by smoking history, body mass index (BMI), and reflux/heartburn.

RESULTS:

After correcting for multiple testing, none of the tested 387 SNPs were statistically significantly associated with risk of EA or Barrett's esophagus. No evidence of effect modification by smoking, BMI, or reflux/heartburn was observed.

CONCLUSIONS:

Genetic risk variants for common cancers identified from GWAS appear not to be associated with risks of EA or Barrett's esophagus.

IMPACT:

To our knowledge, this is the first investigation of pleiotropic genetic associations with risks of EA and Barrett's esophagus.

PMID:
26364162
PMCID:
PMC4648999
DOI:
10.1158/1055-9965.EPI-15-0596
[Indexed for MEDLINE]
Free PMC Article
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