Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001380823 | SCV001579004 | pathogenic | Leber congenital amaurosis 4 | 2022-12-14 | 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: 812218). This premature translational stop signal has been observed in individual(s) with Leber congenital amaurosis (PMID: 20702822). 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.Trp72*) in the AIPL1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in AIPL1 are known to be pathogenic (PMID: 10615133, 15249368, 15347646). |
Gene |
RCV003226992 | SCV003923623 | pathogenic | not provided | 2022-11-02 | criteria provided, single submitter | clinical testing | Identified in a family with Leber congenital amaurosis in the published literature, however detailed segregation data was not provided (Sharon et al., 2020); 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: 31456290) |
Sharon lab, |
RCV001002864 | SCV001160892 | pathogenic | Leber congenital amaurosis | 2019-06-23 | no assertion criteria provided | research |