Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Undiagnosed Diseases Network, |
RCV001598701 | SCV001827218 | pathogenic | Vici syndrome | 2021-04-12 | criteria provided, single submitter | clinical testing | This homozygous deletion at an acceptor site was analyzed in patient cells (with and without puromycin to inhibit NMD) and demonstrated exon skipping of coding exon 35 that was NMD dependent. |
Ai |
RCV002224088 | SCV002502914 | likely pathogenic | not provided | 2022-03-23 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001598701 | SCV004263220 | likely pathogenic | Vici syndrome | 2024-01-11 | criteria provided, single submitter | clinical testing | This sequence change falls in intron 34 of the EPG5 gene. It does not directly change the encoded amino acid sequence of the EPG5 protein. RNA analysis indicates that this variant induces altered splicing and likely disrupts the C-terminus of the protein. This variant is present in population databases (rs773330060, gnomAD 0.01%). This variant has been observed in individual(s) with clinical features of Vici syndrome (PMID: 31226715). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. Studies have shown that this variant results in skipping of exon 35 and introduces a new termination codon (PMID: 31226715). However the mRNA is not expected to undergo nonsense-mediated decay. In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Revvity Omics, |
RCV001598701 | SCV003833529 | uncertain significance | Vici syndrome | 2021-03-12 | flagged submission | clinical testing |