Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000159168 | SCV000209113 | pathogenic | not provided | 2022-07-11 | criteria provided, single submitter | clinical testing | Not observed in large population cohorts (gnomAD); In silico analysis, which includes protein predictors and evolutionary conservation, supports that this variant does not alter protein structure/function; The majority of missense variants in this gene are considered pathogenic (HGMD); This variant is associated with the following publications: (PMID: 24803665, 20648242, 29493581, 17143282, 21387466, 12628188, 20683980, 24077912) |
Center for Genomics, |
RCV003224178 | SCV003920499 | likely pathogenic | Fibromatosis, gingival, 1; Noonan syndrome 4 | 2022-12-29 | criteria provided, single submitter | clinical testing | This variant has been reported in the literature in 3 individuals with clinical suspicion or diagnoses of Noonan syndrome, including at least once as de novo (Longoni 2010 PMID: 20683980; Lepri 2011 PMID: 21387466). It has also been reported in ClinVar, with the only submitting laboratory classifying it as pathogenic (Variation ID: 181552). This variant is absent from gnomAD. This variant is located in the PH domain of the encoded protein, which is recognized as functionally important and is enriched for pathogenic variants in affected individuals (Lepri 2011 PMID: 21387466). Further, missense variation in the SOS1 gene is frequently pathogenic (Gelb 2018 PMID: 29493581). However, evolutionary conservation and computational prediction tools are unclear on the effect of this variant on the protein. In summary, data on this variant is highly suspicious for disease, but requires further evidence for pathogenicity. Therefore, this variant is classified as likely pathogenic. |