Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001387166 | SCV001587726 | pathogenic | Marfan syndrome; Familial thoracic aortic aneurysm and aortic dissection | 2022-01-15 | criteria provided, single submitter | clinical testing | This sequence change replaces tryptophan, which is neutral and slightly polar, with cysteine, which is neutral and slightly polar, at codon 366 of the FBN1 protein (p.Trp366Cys). This variant is not present in population databases (gnomAD no frequency). This missense change has been observed in individuals with Marfan syndrome (PMID: 11700157, 28855619; Invitae). ClinVar contains an entry for this variant (Variation ID: 549004). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt FBN1 protein function. This variant disrupts the p.Trp366 amino acid residue in FBN1. Other variant(s) that disrupt this residue have been observed in individuals with FBN1-related conditions (PMID: 24161884, 29357934), which suggests that this may be a clinically significant amino acid residue. For these reasons, this variant has been classified as Pathogenic. |
Centre of Medical Genetics, |
RCV000663442 | SCV002025422 | likely pathogenic | Marfan syndrome | 2021-03-01 | criteria provided, single submitter | research | PM2, PS1, PP4 |
Center for Medical Genetics Ghent, |
RCV000663442 | SCV000786733 | likely pathogenic | Marfan syndrome | 2017-11-07 | no assertion criteria provided | clinical testing |