Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001659075 | SCV001875282 | pathogenic | not provided | 2024-08-06 | criteria provided, single submitter | clinical testing | Canonical splice site variant predicted to result in an in-frame loss of the adjacent exon in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); Has not been previously published as pathogenic or benign to our knowledge |
Prevention |
RCV004528527 | SCV004104975 | pathogenic | ELN-related disorder | 2023-08-13 | criteria provided, single submitter | clinical testing | The ELN c.800-1G>A variant is predicted to disrupt the AG splice acceptor site and interfere with normal splicing. To our knowledge, this variant has not been reported in the literature or in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Variants that disrupt the consensus splice acceptor site in ELN are expected to be pathogenic and other variants affecting this splice site (c.800-2A>G, c.800-1G>T) have been reported as pathogenic (IVS15-2A>G in Li et al. 1997. PubMed ID: 9215670; Hu et al. 2020. PubMed ID: 32595695). This variant is interpreted as pathogenic. |
Fulgent Genetics, |
RCV005038277 | SCV005667452 | likely pathogenic | Cutis laxa, autosomal dominant 1; Supravalvar aortic stenosis | 2024-02-13 | criteria provided, single submitter | clinical testing |