| Literature DB >> 29696744 |
Ozge Ceyhan-Birsoy1,2, Maya M Miatkowski1, Elizabeth Hynes1, Birgit H Funke1,3, Heather Mason-Suares1,4.
Abstract
RASopathies include a group of syndromes caused by pathogenic germline variants in RAS-MAPK pathway genes and typically present with facial dysmorphology, cardiovascular disease, and musculoskeletal anomalies. Recently, variants in RASopathy-associated genes have been reported in individuals with apparently nonsyndromic cardiomyopathy, suggesting that subtle features may be overlooked. To determine the utility and burden of adding RASopathy-associated genes to cardiomyopathy panels, we tested 11 RASopathy-associated genes by next-generation sequencing (NGS), including NGS-based copy number variant assessment, in 1,111 individuals referred for genetic testing for hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM). Disease-causing variants were identified in 0.6% (four of 692) of individuals with HCM, including three missense variants in the PTPN11, SOS1, and BRAF genes. Overall, 36 variants of uncertain significance (VUSs) were identified, averaging ∼3VUSs/100 cases. This study demonstrates that adding a subset of the RASopathy-associated genes to cardiomyopathy panels will increase clinical diagnoses without significantly increasing the number of VUSs/case.Entities:
Keywords: BRAF; Noonan syndrome; PTPN11; RAF1 gain; RASopathy; SOS1; cardio-facio-cutaneous (CFC) syndrome; dilated cardiomyopathy (DCM); hypertrophic cardiomyopathy (HCM)
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Year: 2018 PMID: 29696744 PMCID: PMC8191452 DOI: 10.1002/humu.23535
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878