Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000080581 | SCV000112483 | pathogenic | not provided | 2017-03-02 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002514414 | SCV003444583 | pathogenic | Duchenne muscular dystrophy | 2021-12-31 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Other variant(s) that result in skipping of exon 25 have been determined to be pathogenic (PMID: 19001018, 19783145). This suggests that this variant may also be clinically significant and likely to be disease-causing. Variants that disrupt the consensus splice site are a relatively common cause of aberrant splicing (PMID: 17576681, 9536098). Studies have shown that this variant results in skipping of exon 25, but is expected to preserve the integrity of the reading-frame (PMID: 18348289). ClinVar contains an entry for this variant (Variation ID: 94592). This variant has been observed in individual(s) with Becker muscular dystrophy (PMID: 18348289; Invitae). This variant is not present in population databases (gnomAD no frequency). This sequence change falls in intron 25 of the DMD gene. It does not directly change the encoded amino acid sequence of the DMD protein. RNA analysis indicates that this variant induces altered splicing and likely results in a shortened protein product. |
Revvity Omics, |
RCV000080581 | SCV003830574 | likely pathogenic | not provided | 2022-01-27 | criteria provided, single submitter | clinical testing |