Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
NIHR Bioresource Rare Diseases, |
RCV001787077 | SCV000899907 | likely pathogenic | von Willebrand disease type 3 | 2019-02-01 | criteria provided, single submitter | research | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV003993804 | SCV004813676 | pathogenic | von Willebrand disorder | 2024-02-06 | criteria provided, single submitter | clinical testing | Variant summary: VWF c.7664_7665insAG (p.Cys2557SerfsX8) results in a premature termination codon, predicted to cause a truncation of the encoded protein or absence of the protein due to nonsense mediated decay, which are commonly known mechanisms for disease. The variant was absent in 251292 control chromosomes. c.7664_7665insAG has been reported in the literature in at least one homozygous individual affected with a coagulation disorder (e.g. Downes_2019). To our knowledge, no experimental evidence demonstrating an impact on protein function has been reported. The following publication has been ascertained in the context of this evaluation (PMID: 31064749). ClinVar contains an entry for this variant (Variation ID: 100481). Based on the evidence outlined above, the variant was classified as pathogenic. |
Academic Unit of Haematology, |
RCV000086895 | SCV000119101 | not provided | not provided | no assertion provided | not provided |