Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008242 | SCV001168008 | pathogenic | not provided | 2022-04-07 | criteria provided, single submitter | clinical testing | Has not been previously published as pathogenic or benign to our knowledge; 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) |
Fulgent Genetics, |
RCV001535995 | SCV001752668 | pathogenic | Leber congenital amaurosis 10; Meckel syndrome, type 4; Senior-Loken syndrome 6; Joubert syndrome 5; Bardet-Biedl syndrome 14 | 2021-06-30 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001860589 | SCV002228477 | pathogenic | Familial aplasia of the vermis; Meckel-Gruber syndrome; Nephronophthisis | 2022-08-09 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu1861Tyrfs*6) 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). This variant has not been reported in the literature in individuals affected with CEP290-related conditions. ClinVar contains an entry for this variant (Variation ID: 817139). For these reasons, this variant has been classified as Pathogenic. This variant is not present in population databases (gnomAD no frequency). |
Natera, |
RCV001827170 | SCV002091864 | likely pathogenic | Leber congenital amaurosis | 2021-06-01 | no assertion criteria provided | clinical testing |