Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Mayo Clinic Laboratories, |
RCV001508887 | SCV001715320 | likely pathogenic | not provided | 2020-04-28 | criteria provided, single submitter | clinical testing | PVS1, PM2 |
Rady Children's Institute for Genomic Medicine, |
RCV001732191 | SCV001984864 | pathogenic | Pyruvate kinase deficiency of red cells | 2020-05-15 | criteria provided, single submitter | clinical testing | This frameshifting variant in exon 3 of 11 introduces a premature stop codon and is therefore predicted to result in loss of normal protein function through either protein truncation or nonsense-mediated mRNA decay (NMD). This variant has not been previously reported or functionally characterized in the literature to our knowledge. It is present in the heterozygous state in the gnomAD population database at a frequency of 0.0004% (1/251388) and thus is presumed to be rare. Based on the available evidence, the c.307del (p.Arg103AlafsTer5) variant is classified as Pathogenic. |
Gene |
RCV001508887 | SCV002765286 | pathogenic | not provided | 2022-06-16 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 7706479, 26832193) |
Revvity Omics, |
RCV001508887 | SCV003822930 | pathogenic | not provided | 2022-09-08 | criteria provided, single submitter | clinical testing |