| Literature DB >> 27225850 |
Atsushi Fujita1, Bertrand Isidor2,3, Hugues Piloquet4, Pierre Corre5, Nobuhiko Okamoto6, Mitsuko Nakashima1, Yoshinori Tsurusaki1, Hirotomo Saitsu1, Noriko Miyake1, Naomichi Matsumoto1.
Abstract
MEIS2 aberrations are considered to be the cause of intellectual disability, cleft palate and cardiac septal defect, as MEIS2 copy number variation is often observed with these phenotypes. To our knowledge, only one nucleotide-level change-specifically, an in-frame MEIS2 deletion-has so far been reported. Here, we report a female patient with a de novo nonsense mutation (c.611C>G, p.Ser204*) in MEIS2. She showed severe intellectual disability, moderate motor/verbal developmental delay, cleft palate, cardiac septal defect, hypermetropia, severe feeding difficulties with gastro-esophageal reflux and constipation. By reviewing this patient and previous patients with MEIS2 point mutations, we found that feeding difficulty with gastro-esophageal reflux appears to be one of the core clinical features of MEIS2 haploinsufficiency, in addition to intellectual disability, cleft palate and cardiac septal defect.Entities:
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Year: 2016 PMID: 27225850 DOI: 10.1038/jhg.2016.54
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172