Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001305509 | SCV001494847 | likely benign | Noonan syndrome 9 | 2025-01-23 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002447309 | SCV002676308 | uncertain significance | Cardiovascular phenotype | 2021-06-23 | criteria provided, single submitter | clinical testing | The p.E422K variant (also known as c.1264G>A), located in coding exon 10 of the SOS2 gene, results from a G to A substitution at nucleotide position 1264. The glutamic acid at codon 422 is replaced by lysine, an amino acid with similar properties. This amino acid position is conserved. In addition, this alteration is predicted to be deleterious by in silico analysis. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Genome- |
RCV001305509 | SCV002763089 | uncertain significance | Noonan syndrome 9 | criteria provided, single submitter | clinical testing | ||
St. |
RCV001305509 | SCV005689320 | uncertain significance | Noonan syndrome 9 | 2025-02-05 | criteria provided, single submitter | clinical testing | The SOS2 c.1264G>A (p.Glu422Lys) missense change has a maximum subpopulation frequency of 0.004% in gnomAD v2.1.1 (https://gnomad.broadinstitute.org/). This variant occurs in a gene where missense variants are more likely to be damaging based on methods described by Lek et al. (PMID: 27535533). The in silico tool REVEL predicts a deleterious effect on protein function, but to our knowledge this prediction has not been confirmed by functional studies. To our knowledge, this variant has not been reported in the literature in individuals with Noonan syndrome. In summary, the evidence currently available is insufficient to determine the clinical significance of this variant. It has therefore been classified as of uncertain significance. |