| Literature DB >> 24736735 |
Florence Démurger1, Amale Ichkou2, Soumaya Mougou-Zerelli3, Martine Le Merrer4, Géraldine Goudefroye2, Anne-Lise Delezoide5, Chloé Quélin1, Sylvie Manouvrier6, Geneviève Baujat7, Mélanie Fradin1, Laurent Pasquier1, André Megarbané8, Laurence Faivre9, Clarisse Baumann10, Sheela Nampoothiri11, Joëlle Roume12, Bertrand Isidor13, Didier Lacombe14, Marie-Ange Delrue14, Sandra Mercier13, Nicole Philip15, Elise Schaefer16, Muriel Holder6, Amanda Krause17, Fanny Laffargue18, Martine Sinico19, Daniel Amram20, Gwenaelle André21, Alain Liquier22, Massimiliano Rossi23, Jeanne Amiel7, Fabienne Giuliano24, Odile Boute6, Anne Dieux-Coeslier6, Marie-Line Jacquemont25, Alexandra Afenjar26, Lionel Van Maldergem27, Marylin Lackmy-Port-Lis28, Catherine Vincent-Delorme29, Marie-Liesse Chauvet30, Valérie Cormier-Daire7, Louise Devisme31, David Geneviève32, Arnold Munnich7, Géraldine Viot33, Odile Raoul2, Serge Romana7, Marie Gonzales34, Ferechte Encha-Razavi35, Sylvie Odent1, Michel Vekemans7, Tania Attie-Bitach7.
Abstract
The phenotypic spectrum of GLI3 mutations includes autosomal dominant Greig cephalopolysyndactyly syndrome (GCPS) and Pallister-Hall syndrome (PHS). PHS was first described as a lethal condition associating hypothalamic hamartoma, postaxial or central polydactyly, anal atresia and bifid epiglottis. Typical GCPS combines polysyndactyly of hands and feet and craniofacial features. Genotype-phenotype correlations have been found both for the location and the nature of GLI3 mutations, highlighting the bifunctional nature of GLI3 during development. Here we report on the molecular and clinical study of 76 cases from 55 families with either a GLI3 mutation (49 GCPS and 21 PHS), or a large deletion encompassing the GLI3 gene (6 GCPS cases). Most of mutations are novel and consistent with the previously reported genotype-phenotype correlation. Our results also show a correlation between the location of the mutation and abnormal corpus callosum observed in some patients with GCPS. Fetal PHS observations emphasize on the possible lethality of GLI3 mutations and extend the phenotypic spectrum of malformations such as agnathia and reductional limbs defects. GLI3 expression studied by in situ hybridization during human development confirms its early expression in target tissues.Entities:
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Year: 2014 PMID: 24736735 PMCID: PMC4266745 DOI: 10.1038/ejhg.2014.62
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246