| Literature DB >> 25824905 |
Maja Sukalo1, Felix Tilsen1, Hülya Kayserili2,3, Dietmar Müller4, Beyhan Tüysüz5, Deborah M Ruddy6, Emma Wakeling7, Karen Helene Ørstavik8, Katie M Snape9, Richard Trembath6,10, Maryse De Smedt11, Nathalie van der Aa12, Martin Skalej13, Stefan Mundlos14, Wim Wuyts12,15, Laura Southgate10,16, Martin Zenker1.
Abstract
Adams-Oliver syndrome (AOS) is characterized by the association of aplasia cutis congenita with terminal transverse limb defects, often accompanied by additional cardiovascular or neurological features. Both autosomal-dominant and autosomal-recessive disease transmission have been observed, with recent gene discoveries indicating extensive genetic heterogeneity. Mutations of the DOCK6 gene were first described in autosomal-recessive cases of AOS and only five DOCK6-related families have been reported to date. Recently, a second type of autosomal-recessive AOS has been attributed to EOGT mutations in three consanguineous families. Here, we describe the identification of 13 DOCK6 mutations, the majority of which are novel, across 10 unrelated individuals from a large cohort comprising 47 sporadic cases and 31 AOS pedigrees suggestive of autosomal-recessive inheritance. DOCK6 mutations were strongly associated with structural brain abnormalities, ocular anomalies, and intellectual disability, thus suggesting that DOCK6-linked disease represents a variant of AOS with a particularly poor prognosis.Entities:
Keywords: AOS; Adams-Oliver syndrome; DOCK6; brain anomalies; eye anomalies
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Year: 2015 PMID: 25824905 DOI: 10.1002/humu.22795
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878