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Cancer Epidemiol Biomarkers Prev. 2017 Oct;26(10):1540-1548. doi: 10.1158/1055-9965.EPI-17-0262. Epub 2017 Jul 28.

Impact of Sixteen Established Pancreatic Cancer Susceptibility Loci in American Jews.

Author information

1
Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut.
2
Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland.
3
Department of Pathology, Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, Maryland.
4
Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York.
5
Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.
6
Department of Biostatistics, Yale School of Public Health, New Haven, Connecticut.
7
Program of Computational Biology and Bioinformatics, Yale University, New Haven, Connecticut.
8
Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut. harvey.risch@yale.edu.

Abstract

Background: The higher risk of pancreatic cancer in Ashkenazi Jews compared with non-Jews is only partially explained by the increased frequency of BRCA1 and BRCA2 mutations in Ashkenazi Jews.Methods: We evaluated the impact of 16 established pancreatic cancer susceptibility loci in a case-control sample of American Jews, largely Ashkenazi, including 406 full-Jewish pancreatic cancer patients and 2,332 full-Jewish controls, genotyped as part of the Pancreatic Cancer Cohort and Case-Control Consortium I/II (PanScan I/II), Pancreatic Cancer Case-Control Consortium (PanC4), and Resource for Genetic Epidemiology Research on Adult Health and Aging (GERA) datasets. We compared risk in full-Jewish subjects with risk in part-Jewish; non-Jewish Southern European; and in the combined non-Jewish Eastern, Northern, Southern, and Western European (non-Jewish white European) subjects from the same datasets. Jewish ancestries were genetically identified using seeded Fast principal component analysis. Data were analyzed by unconditional logistic regression, and adjusted for age, sex, and principal components.Results: One SNP on chromosome 13q22.1 (rs9543325; OR, 1.36; 95% confidence interval, 1.16-1.58; P = 10-4.1) was significant in full-Jews. Individual ORs and minor allele frequencies were similar between Jewish and non-Jewish white European subjects. The average ORs across the 16 pancreatic cancer susceptibility loci for full-Jewish, full- plus part-Jewish, non-Jewish Southern European, and non-Jewish white European subjects were 1.25, 1.30, 1.31, and 1.26, respectively.Conclusions: The 16 pancreatic cancer susceptibility loci similarly impact Jewish and non-Jewish white European subjects, both individually and as summary odds.Impact: These 16 pancreatic cancer susceptibility loci likely do not explain the higher risk seen in Ashkenazi Jews. Cancer Epidemiol Biomarkers Prev; 26(10); 1540-8. ©2017 AACR.

PMID:
28754795
PMCID:
PMC5626623
[Available on 2018-10-01]
DOI:
10.1158/1055-9965.EPI-17-0262
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