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Publication Information
Affiliation
Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Center for Public Health Genomics, University of Virginia, Charlottesville, VA.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Pacific Northwest Diabetes Research Institute, Seattle, WA.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K.; Pacific Northwest Diabetes Research Institute, Seattle, WA r.oram@exeter.ac.uk wah@uw.edu.; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, U.K. r.oram@exeter.ac.uk wah@uw.edu.
Authors
Sharp Seth A, Rich Stephen S, Wood Andrew R, Jones Samuel E, Beaumont Robin N, Harrison James W, Schneider Darius A, Locke Jonathan M, Tyrrell Jess, Weedon Michael N, Hagopian William A, Oram Richard A
Studies
Abstract
Previously generated genetic risk scores (GRSs) for type 1 diabetes (T1D) have not captured all known information at non-HLA loci or, particularly, at HLA risk loci. We aimed to more completely incorporate HLA alleles, their interactions, and recently discovered non-HLA loci into an improved T1D GRS (termed the "T1D GRS2") to better discriminate diabetes subtypes and to predict T1D in newborn screening studies.