| Literature DB >> 25374402 |
Mitsuko Nakashima1, Masakazu Miyajima2, Hidenori Sugano2, Yasushi Iimura2, Mitsuhiro Kato3, Yoshinori Tsurusaki1, Noriko Miyake1, Hirotomo Saitsu1, Hajime Arai2, Naomichi Matsumoto1.
Abstract
Sturge-Weber syndrome (SWS) is a neurocutaneous disorder characterized by capillary malformation (port-wine stains), and choroidal and leptomeningeal vascular malformations. Previously, the recurrent somatic mutation c.548G>A (p.R183Q) in the G-α q gene (GNAQ) was identified as causative in SWS and non-syndromic port-wine stain patients using whole-genome sequencing. In this study, we investigated somatic mutations in GNAQ by next-generation sequencing. We first performed targeted amplicon sequencing of 15 blood-brain-paired samples in sporadic SWS and identified the recurrent somatic c.548G>A mutation in 80% of patients (12 of 15). The percentage of mutant alleles in brain tissues of these 12 patients ranged from 3.6 to 8.9%. We found no other somatic mutations in any of the seven GNAQ exons in the remaining three patients without c.548G>A. These findings suggest that the recurrent somatic GNAQ mutation c.548G>A is the major determinant genetic factor for SWS and imply that other mutated candidate gene(s) may exist in SWS.Entities:
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Year: 2014 PMID: 25374402 DOI: 10.1038/jhg.2014.95
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172