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Diabetes 53:2479-2482, 2004
© 2004 by the American Diabetes Association, Inc.

Brief Genetics Report

Association Analysis of the Lymphocyte-Specific Protein Tyrosine Kinase (LCK) Gene in Type 1 Diabetes

John S. Hulme1, Bryan J. Barratt1, Rebecca C.J. Twells1, Jason D. Cooper1, Chris E. Lowe1, Joanna M.M. Howson1, Alex C. Lam1, Luc J. Smink1, David A. Savage2, Dag E. Undlien3, Cristian Guja4, Constantin Ionescu-Tîirgoviste4, Eva Tuomilehto-Wolf5, Jaakko Tuomilehto5,6, and John A. Todd1

1 Juvenile Diabetes Research Foundation (JDRF)/Wellcome Trust (WT) Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, U.K
2 Department of Medical Genetics, Queen’s University Belfast, Belfast City Hospital, Belfast, Northern Ireland
3 Institute of Medical Genetics, Ulleval University Hospital, University of Oslo, Oslo, Norway
4 Clinic of Diabetes, Institute of Diabetes, Nutrition, and Metabolic Diseases ‘N. Paulescu’, Bucharest, Romania
5 Diabetes and Genetic Epidemiology Unit, National Public Health Institute, University of Helsinki, Helsinki, Finland
6 Department of Public Health, University of Helsinki, Helsinki, Finland

Prior data associating the expression of lymphocyte-specific protein tyrosine kinase (LCK) with type 1 diabetes, its critical function in lymphocytes, and the linkage of the region to diabetes in the nonobese diabetic (NOD) mouse model make LCK a premier candidate for a susceptibility gene. Resequencing of LCK in 32 individuals detected seven single nucleotide polymorphisms (SNPs) with allele frequencies >3%, including four common SNPs previously reported. These and six other SNPs from dbSNP were genotyped in a two-stage strategy using 2,430 families and were all shown not to be significantly associated with type 1 diabetes. We conclude that a major role for the common LCK polymorphisms in type 1 diabetes is unlikely. However, we cannot rule out the possibility of there being a causal variant outside the exonic, intronic, and untranslated regions studied.

Address correspondence and reprint requests to Prof. John A. Todd, JDRF/WT Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, Wellcome Trust/MRC Building, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 2XY, U.K. E-mail: john.todd{at}cimr.cam.ac.uk


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Copyright © 2004 by the American Diabetes Association.