| Literature DB >> 30430033 |
Fernando Rodríguez1, Carla Vallejos1, Víctor M Bolanos-Garcia2, Diana Ponce1, Nancy Unanue1, Francisco Garay3, Fernando Cassorla1, Mariana Aracena3,4.
Abstract
We report the case of a 3-year-old girl, who is the third child of nonconsanguineous parents, with short stature, hypertrophic cardiomyopathy, and mild dysmorphic features; all suggestive of Noonan syndrome. In addition, the patient presents with feeding difficulties, deep palmar and plantar creases, sparse hair, and delayed psychomotor and language development, all characteristics frequently observed in cardiofaciocutaneous syndrome. Molecular analysis of the Ras/ MAPK pathway genes using high-resolution melting curve analysis and gene sequencing revealed a de novo KRAS amino acid substitution of leucine to tryptophan at codon 53 (p.L53W). This substitution was recently described in an Iranian patient with Noonan syndrome. The findings described in this report expand the phenotypic heterogeneity observed in RASopathy patients harboring a KRAS substitution, and advocate for the inclusion of genes with low mutational frequency in genetic screening protocols for Noonan syndrome and other RASopathies.Entities:
Keywords: KRAS mutations ; Noonan syndrome; cardiofaciocutaneous syndrome
Year: 2018 PMID: 30430033 PMCID: PMC6234039 DOI: 10.1055/s-0038-1653977
Source DB: PubMed Journal: J Pediatr Genet ISSN: 2146-460X