Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV004595853 | SCV005088576 | pathogenic | RPE65-related recessive retinopathy | 2024-07-23 | reviewed by expert panel | curation | NM_000329.3(RPE65):c.138del (p.Pro47GlnfsTer47) is a frameshift variant that introduces a premature stop codon into exon 3 of 14, and is predicted to lead to nonsense-mediated decay in a gene in which loss-of-function is an established mechanism of disease (PVS1). This variant is absent from gnomAD v2.1.1 (PM2_Supporting). This variant has been reported in at least 2 unrelated probands with early-onset severe retinal dystrophy who were homozygous for the variant (1 point, PMID: 36017377, PM3). In summary, this variant meets the criteria to be classified as pathogenic for RPE65-related recessive retinopathy based on the ACMG/AMP criteria applied, as specified by the ClinGen LCA / eoRD VCEP: PVS1, PM2_supporting, and PM3. (VCEP specifications version 1.0.0; date of approval 09/21/2023) |
Baylor Genetics | RCV001250677 | SCV005055430 | pathogenic | Leber congenital amaurosis 2 | 2024-03-30 | criteria provided, single submitter | clinical testing | |
Retina International | RCV000085170 | SCV000117307 | not provided | not provided | no assertion provided | not provided | ||
Laboratory of Genetics in Ophthalmology, |
RCV001250677 | SCV001425547 | pathogenic | Leber congenital amaurosis 2 | no assertion criteria provided | research |