Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000579059 | SCV000680729 | pathogenic | not provided | 2022-08-02 | criteria provided, single submitter | clinical testing | Nonsense 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: 25525159, 31589614, 20079931, 28829391, 17345604) |
Labcorp Genetics |
RCV002530367 | SCV003441210 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome; Nephronophthisis | 2023-07-31 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 488821). This premature translational stop signal has been observed in individual(s) with Leber congenital amaurosis (PMID: 17345604). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This sequence change creates a premature translational stop signal (p.Ser570*) in the CEP290 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CEP290 are known to be pathogenic (PMID: 16909394, 17345604, 20690115). |
Baylor Genetics | RCV003459415 | SCV004214820 | pathogenic | Bardet-Biedl syndrome 14 | 2024-02-11 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics, |
RCV004817775 | SCV005070485 | pathogenic | Retinal dystrophy | 2015-01-01 | criteria provided, single submitter | clinical testing |