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2 results on '"Thun GA"'

1. Novel childhood asthma genes interact with in utero and early-life tobacco smoke exposure.

Author

Scholtens S, Postma DS, Moffatt MF, Panasevich S, Granell R, Henderson AJ, Melén E, Nyberg F, Pershagen G, Jarvis D, Ramasamy A, Wjst M, Svanes C, Bouzigon E, Demenais F, Kauffmann F, Siroux V, von Mutius E, Ege MJ, Braun-Fahrländer C, Genuneit J, Brunekreef B, Smit HA, Wijga AH, Kerkhof M, Curjuric I, Imboden M, Thun GA, Probst-Hensch N, Freidin MB, Bragina EIu, Deev IA, Puzyrev VP, Daley D, Park J, Becker A, Chan-Yeung M, Kozyrskyj AL, Pare P, Marenholz I, Lau S, Keil T, Lee YA, Kabesch M, Wijmenga C, Franke L, Nolte IM, Vonk J, Kumar A, Farrall M, Cookson WO, Strachan DP, Koppelman GH, and Boezen HM

Subjects
Female, Humans, Microfilament Proteins genetics, Polymorphism, Single Nucleotide, Asthma etiology, Asthma genetics, Gene-Environment Interaction, Maternal Exposure adverse effects, Tobacco Smoke Pollution adverse effects
Published
2014
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2. Genome-wide association study of lung function decline in adults with and without asthma.

Author

Imboden M, Bouzigon E, Curjuric I, Ramasamy A, Kumar A, Hancock DB, Wilk JB, Vonk JM, Thun GA, Siroux V, Nadif R, Monier F, Gonzalez JR, Wjst M, Heinrich J, Loehr LR, Franceschini N, North KE, Altmüller J, Koppelman GH, Guerra S, Kronenberg F, Lathrop M, Moffatt MF, O'Connor GT, Strachan DP, Postma DS, London SJ, Schindler C, Kogevinas M, Kauffmann F, Jarvis DL, Demenais F, and Probst-Hensch NM

Subjects
Adult, Asthma diagnosis, Asthma physiopathology, Europe, Female, Follow-Up Studies, Forced Expiratory Volume, Humans, Lung pathology, Male, Membrane Proteins genetics, Middle Aged, Neoplasm Proteins, Polymorphism, Single Nucleotide, Tumor Suppressor Proteins genetics, Vital Capacity, Young Adult, Asthma epidemiology, Asthma genetics, Chromosomes, Human, Pair 13 genetics, Genome-Wide Association Study, Lung metabolism
Abstract

Background: Genome-wide association studies have identified determinants of chronic obstructive pulmonary disease, asthma, and lung function level; however, none have addressed decline in lung function., Objective: We conducted the first genome-wide association study on the age-related decrease in FEV(1) and its ratio to forced vital capacity (FVC) stratified a priori by asthma status., Methods: Discovery cohorts included adults of European ancestry (1,441 asthmatic and 2,677 nonasthmatic participants: the Epidemiological Study on the Genetics and Environment of Asthma, the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults, and the European Community Respiratory Health Survey). The associations of FEV(1) and FEV(1)/FVC ratio decrease with 2.5 million single nucleotide polymorphisms (SNPs) were estimated. Thirty loci were followed up by in silico replication (1,160 asthmatic and 10,858 nonasthmatic participants: Atherosclerosis Risk in Communities, the Framingham Heart Study, the British 1958 Birth Cohort, and the Dutch Asthma Study)., Results: Main signals identified differed between asthmatic and nonasthmatic participants. None of the SNPs reached genome-wide significance. The association between the height-related gene DLEU7 and FEV(1) decrease suggested for nonasthmatic participants in the discovery phase was replicated (discovery, P = 4.8 × 10(-6); replication, P = .03), and additional sensitivity analyses point to a relation to growth. The top ranking signal, TUSC3, which is associated with FEV(1)/FVC ratio decrease in asthmatic participants (P = 5.3 × 10(-8)), did not replicate. SNPs previously associated with cross-sectional lung function were not prominently associated with decline., Conclusions: Genetic heterogeneity of lung function might be extensive. Our results suggest that genetic determinants of longitudinal and cross-sectional lung function differ and vary by asthma status., (Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.)

Published
2012
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