Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV002265502 | SCV002547236 | uncertain significance | not provided | 2022-01-10 | criteria provided, single submitter | clinical testing | Missense variants in this gene are often considered pathogenic (HGMD); In silico analysis supports that this missense variant does not alter protein structure/function; Has not been previously published as pathogenic or benign to our knowledge; This variant is associated with the following publications: (PMID: 29493581) |
Fulgent Genetics, |
RCV002488661 | SCV002785638 | uncertain significance | Fibromatosis, gingival, 1; Noonan syndrome 4 | 2021-07-23 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003096001 | SCV003519515 | likely benign | RASopathy | 2023-01-02 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV005281157 | SCV005947549 | uncertain significance | Cardiovascular phenotype | 2025-01-06 | criteria provided, single submitter | clinical testing | The p.E590D variant (also known as c.1770G>C), located in coding exon 10 of the SOS1 gene, results from a G to C substitution at nucleotide position 1770. The glutamic acid at codon 590 is replaced by aspartic acid, an amino acid with highly similar properties. This amino acid position is conserved. In addition, this alteration is predicted to be tolerated by in silico analysis. Based on the available evidence, the clinical significance of this variant remains unclear. |