Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001916691 | SCV002191674 | pathogenic | Marfan syndrome; Familial thoracic aortic aneurysm and aortic dissection | 2022-02-05 | criteria provided, single submitter | clinical testing | This variant is not present in population databases (gnomAD no frequency). For these reasons, this variant has been classified as Pathogenic. 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 missense change has been observed in individual(s) with clinical features of Marfan syndrome (Invitae). This sequence change replaces glutamic acid, which is acidic and polar, with lysine, which is basic and polar, at codon 1769 of the FBN1 protein (p.Glu1769Lys). |
Department of Laboratory Medicine and Genetics, |
RCV005050463 | SCV005684890 | likely pathogenic | Marfan syndrome | 2025-01-02 | no assertion criteria provided | clinical testing | The NM_000138.5:c.5305G>A is considered to be rare in the general population database (gnomAD v2.1.1). This variant is predicted to be deletrious by in-silico analysis (REVEL). This variant is located in functional domains. This variant was found in a patient with known Marfan syndrome (PMID: 11933199). In summary, this variant was classified as a likely pathogenic variant for Marfan syndrome (PM1, PP2, PP3, PS4_P, PM2_P). |