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Noonan syndrome is the most common RASopathy and is associated with high rates of neurodevelopmental disorders. Prior neuroimaging studies in children with Noonan syndrome have identified structural effects on subcortical regions, though most focus on volumetric differences, overlooking finer morphological changes. These studies also tend to examine common genetic variants, excluding rarer forms within the Noonan syndrome spectrum. Shape analysis offers a sensitive approach to detecting subtle alterations, and when applied across variants, may reveal distinct neuroanatomical signatures. We acquired anatomical magnetic resonance imaging scans from 104 children with Noonan syndrome spectrum (ages 5 to 17, mean = 10.0) and 80 age- and sex-matched typically developing children (ages 4 to 16, mean = 9.54). Our comprehensive analysis examined local thickness and surface dilation/contraction (Jacobian), including genetic variant-specific analyses. Noonan syndrome spectrum showed widespread subcortical alterations beyond volume reduction, including thinning and surface contraction in the putamen, pallidum, thalamus, and caudate, and expansion in the accumbens. Distinct regional effects were found for PTPN11, SOS1, and other Noonan syndrome spectrum-associated variants. These findings confirm subcortical volume reductions in several regions and highlight complex, region-specific shape alterations. Importantly, neuroanatomical patterns varied across genetic variants, suggesting distinct mechanisms of brain development. Understanding these variant-specific structural profiles may provide insights into genotype-based approaches and inform future precision medicine strategies.
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http://dx.doi.org/10.1093/cercor/bhaf217 | DOI Listing |
JAACAP Open
September 2025
Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands.
Objective: The current study aims to examine executive and social functioning in children and adolescents with Noonan syndromes, which contributes to the understanding of the cognitive and behavioral profile of this population and possible treatment options.
Method: A total of 26 children and adolescents with Noonan syndromes (including Noonan syndrome, Noonan syndrome with multiple lentigines, and Noonan-like syndrome with loose anagen hair; mean age = 11.92 years, SD = 2.
Circ Cardiovasc Interv
September 2025
Division of Cardiology (Y.D., E.P., L.B., M.J.G., R.C., J.T., M.L.O.B., D.V., A.G.D.W., E.F., R.S., J.J.R., C.L.S.), Children's Hospital of Philadelphia, PA.
Background: External drainage of the thoracic duct can temporarily reduce tissue congestion and improve symptoms in patients with heart failure. However, loss of fluid limits the duration of this approach. Here, we report on our initial experience with thoracic duct drainage and autotransfusion in patients with elevated central venous pressure.
View Article and Find Full Text PDFJCEM Case Rep
October 2025
Department of Pediatrics, Rhode Island Hospital/Hasbro Children's, Brown University Health, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA.
Individuals with Noonan syndrome (NS) are predisposed to hematologic cancers, solid tumors, and low-grade gliomas. We report an 8-year-old girl originally referred at age 14 months for short stature, developmental delay, and failure to thrive who was subsequently found to have pathogenetic variants both in and Family history included a maternal half-sister with NS and a mother carrying the mutation. Familial single-gene testing showed a heterozygous pathogenic variant in (c.
View Article and Find Full Text PDFJ Pediatr Hematol Oncol
August 2025
Adolescent and Young Adult Oncology, Division of Hematology-Oncology, Seattle Children's Hospital, University of Washington.
Maxillofacial giant cell lesions (MGCLs) can lead to disfigurement and functional impairments. Management often involves a combination of operative and nonoperative strategies. This case series presents the first reported use of imatinib for multifocal MGCLs in a patient with Noonan syndrome, alongside 2 patients with cherubism.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520.
Noonan syndrome with multiple lentigines (NSML) is a rare autosomal dominant disorder caused by mutations in (protein tyrosine phosphatase nonreceptor type 11) which encodes for the protein tyrosine phosphatase, SHP2. Approximately 85% of NSML patients develop hypertrophic cardiomyopathy (HCM). Here, we show that SHP2 is recruited to tyrosyl phosphorylated protein-zero related (PZR) in NSML mice.
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