TY - JOUR
T1 - Association of Forced Vital Capacity with the Developmental Gene NCOR2
AU - Minelli, C.
AU - Dean, C.H.
AU - Hind, M.
AU - Alves, A.C.
AU - Amaral, A.F.S.
AU - Siroux, V.
AU - Huikari, V.
AU - Artigas, M.S.
AU - Evans, D.M.
AU - Loth, D.W.
AU - Bossé, Y.
AU - Postma, D.S.
AU - Sin, D.
AU - Thompson, J.
AU - Demenais, F.
AU - Henderson, J.
AU - Bouzigon, E.
AU - Jarvis, D.
AU - Järvelin, M.R.
AU - Burney, P.
AU - CHARGE consortium
AU - SpiroMeta consortium
AU - James, Alan L.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - © 2016 Minelli et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Background Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. Methods Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 children (ALSPAC). Associations were considered replicated if the replication p-value survived Bonferroni correction (p
AB - © 2016 Minelli et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Background Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. Methods Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 children (ALSPAC). Associations were considered replicated if the replication p-value survived Bonferroni correction (p
U2 - 10.1371/journal.pone.0147388
DO - 10.1371/journal.pone.0147388
M3 - Article
C2 - 26836265
SN - 1932-6203
VL - 11
JO - PLoS One
JF - PLoS One
IS - 2
M1 - e0147388
ER -