Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000198829 | SCV000250220 | uncertain significance | not provided | 2023-03-09 | criteria provided, single submitter | clinical testing | In silico analysis supports that this missense variant does not alter protein structure/function; Does not affect a cysteine residue within a calcium-binding EGF-like domain of the FBN2 gene; cysteine substitutions in the calcium-binding EGF-like domains represent the majority of pathogenic missense changes associated with FBN2-related disorders (Collod-Beroud et al., 2003; Frederic et al., 2009).; Has not been previously published as pathogenic or benign to our knowledge |
Labcorp Genetics |
RCV000463573 | SCV000553171 | likely benign | Congenital contractural arachnodactyly | 2025-01-29 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002315585 | SCV000738947 | uncertain significance | Familial thoracic aortic aneurysm and aortic dissection | 2024-04-22 | criteria provided, single submitter | clinical testing | The p.K1759Q variant (also known as c.5275A>C), located in coding exon 41 of the FBN2 gene, results from an A to C substitution at nucleotide position 5275. The lysine at codon 1759 is replaced by glutamine, an amino acid with similar properties. This amino acid position is highly conserved in available vertebrate species. 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. |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV003987442 | SCV004804259 | likely benign | not specified | 2024-01-08 | criteria provided, single submitter | clinical testing |