Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
NIHR Bioresource Rare Diseases, |
RCV000852003 | SCV000899445 | likely pathogenic | Hypofibrinogenemia | 2019-02-01 | criteria provided, single submitter | research | |
Institute of Human Genetics, |
RCV002067219 | SCV002496147 | pathogenic | Familial dysfibrinogenemia | 2022-01-20 | criteria provided, single submitter | clinical testing | ACMG categories: PVS1,PM2,PP5 |
Fulgent Genetics, |
RCV005029421 | SCV005662398 | pathogenic | Familial visceral amyloidosis, Ostertag type; Congenital afibrinogenemia; Familial dysfibrinogenemia | 2024-05-17 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004735797 | SCV005362251 | pathogenic | FGA-related disorder | 2024-08-14 | no assertion criteria provided | clinical testing | The FGA c.117delT variant is predicted to result in a frameshift and premature protein termination (p.Val40Trpfs*31). This variant has been reported, along with the common FGA 11kb del and in the homozygous state, in individuals with congenital afibrinogenemia (Reported as g.1185delT, Neerman-Arbez et al. 2001. PubMed ID: 11354637; Hadjali-Saichi et al. 2022. PubMed ID: 35488806). It was also reported to partially contribute to the phenotype in another individual with thrombotic disease (Supplementary Table 3, Downes et al. 2019. PubMed ID: 31064749). This variant is reported in 0.0062% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Frameshift variants in FGA are expected to be pathogenic. This variant is interpreted as pathogenic. |