Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001539717 | SCV001757520 | pathogenic | not provided | 2025-01-08 | 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: 22508176, 36938073) |
Juno Genomics, |
RCV004796639 | SCV005417965 | pathogenic | Polycystic kidney disease, adult type | criteria provided, single submitter | clinical testing | PVS1+PM2_Supporting+PS4_Supporting+PP4 | |
Fulgent Genetics, |
RCV004796639 | SCV005643162 | likely pathogenic | Polycystic kidney disease, adult type | 2024-05-31 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV003900787 | SCV004710342 | pathogenic | PKD1-related disorder | 2023-10-24 | no assertion criteria provided | clinical testing | The PKD1 c.2038delT variant is predicted to result in a frameshift and premature protein termination (p.Tyr680Metfs*105). This variant was reported in an individual with autosomal dominant polycystic kidney disease (ADPKD) (Audrézet et al. 2012. PubMed ID: 22508176, Supp. Table S4). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Frameshift variants in PKD1 are expected to be pathogenic. This variant is interpreted as pathogenic. |