Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Institute of Medical Genetics and Applied Genomics, |
RCV001543446 | SCV001762020 | pathogenic | not provided | 2021-06-17 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001543446 | SCV002601564 | pathogenic | not provided | 2022-05-13 | 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); Identified in a family with clinical features and inheritance suggestive of X-linked retinitis pigmentosa in published literature; reported as 1275_1276delCT (Bader et al., 2003); This variant is associated with the following publications: (PMID: 12657579) |
Prevention |
RCV001543446 | SCV002759621 | pathogenic | not provided | 2017-08-02 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003538637 | SCV004299799 | pathogenic | Primary ciliary dyskinesia | 2023-03-08 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu406Ilefs*46) in the RPGR gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in RPGR are known to be pathogenic (PMID: 16055928, 16969763). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with clinical features of RPGR-related conditions (PMID: 12657579, 34985506). This variant is also known as 1275_1276delCT (L406fsX451). For these reasons, this variant has been classified as Pathogenic. |
Blueprint Genetics | RCV001251554 | SCV001427262 | pathogenic | Retinitis pigmentosa 3 | no assertion criteria provided | clinical testing |