A genome-wide screen for nicotine dependence susceptibility loci

Genome‐wide model free linkage analysis was conducted for nicotine dependence and tobacco use phenotypes in 607 members of 158 nuclear families consisting of at least two ever smokers (100 or more cigarettes smoked in lifetime). DNA from whole blood was genotyped for 739 autosomal microsatellite pol...

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Published inAmerican journal of medical genetics. Part B, Neuropsychiatric genetics Vol. 141B; no. 4; pp. 354 - 360
Main Authors Swan, Gary E., Hops, Hyman, Wilhelmsen, Kirk C., Lessov-Schlaggar, Christina N., Cheng, Li S.-C., Hudmon, Karen S., Amos, Christopher I., Feiler, Heidi S., Ring, Huijun Z., Andrews, Judy A., Tildesley, Elizabeth, Benowitz, Neal
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 05.06.2006
Wiley-Liss
Subjects
Biological and medical sciences
dependence
Family Health
Female
Genetic Linkage
Genetic Predisposition to Disease - genetics
Genetic Testing - methods
genetics
Genome, Human
Humans
linkage
Lod Score
Male
Medical genetics
Medical sciences
Microsatellite Repeats - genetics
nicotine
Nuclear Family
Pedigree
Quantitative Trait Loci - genetics
smoking
Tobacco Use Disorder - diagnosis
Tobacco Use Disorder - genetics
Pathogenesis
Dependence
Predisposition
Genome
Locus
Genetic determinism
Nicotine
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Summary:Genome‐wide model free linkage analysis was conducted for nicotine dependence and tobacco use phenotypes in 607 members of 158 nuclear families consisting of at least two ever smokers (100 or more cigarettes smoked in lifetime). DNA from whole blood was genotyped for 739 autosomal microsatellite polymorphisms with an average inter‐marker distance of 4.6 cM. A peak LOD score of 2.7 was observed on chromosome 6 for scores for the Fagerström Test for Nicotine Dependence. Exploratory analyses were conducted to determine whether sequence variation at other loci affected other measures of dependence or tobacco use. Four additional loci with LOD scores of 2.7 or more were associated with alternative measures of nicotine dependence, one with current frequency of use, and one with smoking cessation. Several of the corresponding support intervals were near putative loci reported previously (on chromosomes 6, 7, and 8) while others appear to be novel (on chromosomes 5, 16, and 19). © 2006 Wiley‐Liss, Inc.
Bibliography:Funds from the State of California for medical research on alcohol and substance abuse through the Department of Neurology of University of California at San Francisco
Gary E. Swan, Hyman Hops, and Kirk C. Wilhelmsen contributed equally to the conduct of this research.
The National Institute of Drug Abuse - No. DA03706
istex:3A8191A3AD6A01F43B8FFC92FB537142AAA9A636
The University of California Tobacco-Related Diseases Research Program - No. 7PT2000, 2001, 2002, 2003, 2004
ArticleID:AJMG30315
ark:/67375/WNG-95D40LNG-R
Please cite this article as follows: Swan GE, Hops H, Wilhelmsen KC, Lessov-Schlaggar CN, Cheng LS-C, Hudmon KS, Amos CI, Feiler HS, Ring HZ, Andrews JA, Tildesley E, Benowitz N. 2006. A Genome-Wide Screen for Nicotine Dependence Susceptibility Loci. Am J Med Genet Part B 141B:354-360.
Please cite this article as follows: Swan GE, Hops H, Wilhelmsen KC, Lessov‐Schlaggar CN, Cheng LS‐C, Hudmon KS, Amos CI, Feiler HS, Ring HZ, Andrews JA, Tildesley E, Benowitz N. 2006. A Genome‐Wide Screen for Nicotine Dependence Susceptibility Loci. Am J Med Genet Part B 141B:354–360.
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These three authors contributed equally to the conduct of this research.
Current affiliation for KCW: Department of Genetics and Neurology, University of North Carolina, Chapel Hill; KSH: Department of Epidemiology and Public Health, Yale University School of Medicine; HSF: Department of Laboratory Medicine, University of California San Francisco and Lawrence Berkeley National Laboratory
ISSN:1552-4841
1552-485X
DOI:10.1002/ajmg.b.30315