Absence of linkage between inflammatory bowel disease and selected loci on chromosomes 3,7,12, and 16.
Background & Aims
Linkage data derived from genome-wide scans of inflammatory bowel disease (IBD) sibling-pair families have identified 4 loci on chromosomes 3,7,12, and 16 as potential sites for IBD susceptibility genes.
The aim of this study was to investigate whether linkage analysis of another independently collected set of sibling pairs with IBD would provide further evidence of linkage between these previously reported loci and IBD.
Using the MAPMAKER/SIBS program, the segregation of 21 microsatellite marker loci spanning the 4 putative IBD gene loci was analyzed in a study population comprising 161 families with 114 Crohn's disease, 36 ulcerative colitis, and 50 mixed IBD sibling pairs from the Greater Toronto area.
The results of multipoint linkage analysis showed no evidence for linkage between IBD and each of the 21 marker loci studied ; the logarithm of odds scores in all instances were less than 0.8. These linkage data were found, by exclusion mapping analysis, to exclude values of As ranging from 1.5 to 3.0, depending on the locus evaluated.
The loci previously suggested as representing IBD susceptibility loci are not linked to IBD in the Toronto population examined in this analysis.
Mots-clés Pascal : Rectocolite ulcérohémorragique, Entérite Crohn, Colite, Prédisposition, Liaison génétique, Chromosome A3, Chromosome C7, Chromosome C12, Chromosome E16, Etude statistique, Homme, Canada, Amérique du Nord, Amérique, Appareil digestif pathologie, Intestin pathologie, Maladie inflammatoire, Génétique
Mots-clés Pascal anglais : Ulcerative colitis, Crohn disease, Colitis, Predisposition, Linkage, Chromosome A3, Chromosome C7, Chromosome C12, Chromosome E16, Statistical study, Human, Canada, North America, America, Digestive diseases, Intestinal disease, Inflammatory disease, Genetics
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 98-0526097
Code Inist : 002B13B03. Création : 23/03/1999.