Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
NIHR Bioresource Rare Diseases, |
RCV000851993 | SCV000899434 | likely pathogenic | Hypofibrinogenemia | 2019-02-01 | criteria provided, single submitter | research | |
Mayo Clinic Laboratories, |
RCV002284177 | SCV002573727 | likely pathogenic | not provided | 2024-06-05 | criteria provided, single submitter | clinical testing | PP1_strong, PM1_supporting, PM2_moderate, PS4_moderate |
Center for Genomic Medicine, |
RCV002284177 | SCV005090626 | likely pathogenic | not provided | 2025-03-04 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000017843 | SCV000038122 | other | FIBRINOGEN AARHUS 1 | 2012-12-20 | no assertion criteria provided | literature only | |
Prevention |
RCV004734521 | SCV005352553 | pathogenic | FGA-related disorder | 2024-07-11 | no assertion criteria provided | clinical testing | The FGA c.112A>G variant is predicted to result in the amino acid substitution p.Arg38Gly. This variant, previously reported as Fibrinogen Milano XIII and as p.Arg19Gly using legacy nomenclature, has been reported to be causative for autosomal dominant dysfibrinogenemia (Bolliger-Stucki et al. 1999. PubMed ID: 10605955; Table S3, Downes et al. 2019. PubMed ID: 31064749; Asselta et al. 2015. PubMed ID: 26006300). This variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD. This variant is interpreted as pathogenic. |