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Costello syndrome is a rare autosomal dominant RASopathy characterized by failure to thrive, severe hypotonia, and predisposition to tumors. Germline missense variants in KRAS have been reported in five unrelated individuals with clinical features of Costello syndrome: a de novo c.466T>G (p.Phe156Val) (PMID:17601930), two cases among 31 patients with cardio-facio-cutaneous and Costello syndrome (PMID:18042262), and two among 260 individuals screened for KRAS mutations (PMID:17056636). All occurred de novo with no reported familial segregation.
Functional studies demonstrate that these KRAS mutants stabilize the GTP-bound active conformation, enhance intrinsic nucleotide exchange, and dysregulate downstream MAPK signaling in vitro (PMID:17875937). Structural modeling of C-terminal isoform-specific mutations (e.g., p.Asp153Val) predicts perturbation of the guanine-binding pocket and increased GTP affinity (PMID:16773572). These data provide moderate functional evidence for a gain-of-function mechanism. No studies have refuted this association.
Key Take-home: Germline KRAS missense variants cause a de novo, autosomal dominant form of Costello syndrome, with limited genetic data and concordant functional validation supporting clinical testing in RASopathy patients.
Gene–Disease AssociationLimited5 unrelated probands (all de novo) across 3 studies; no segregation data; functional concordance Genetic EvidenceLimited5 missense variants in KRAS identified in 5 individuals with Costello syndrome; de novo occurrence Functional EvidenceModerateIn vitro assays show KRAS mutants increase GTP-bound active conformation and downstream MAPK signaling ([PMID:17875937], [PMID:16773572]) |