Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000760550 | SCV000890441 | pathogenic | not provided | 2020-09-18 | criteria provided, single submitter | clinical testing | Reported previously in association with Duchenne muscular dystrophy (Okubo et al., 2017); 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 in large population cohorts (Lek et al., 2016); Based on the understanding of this genetic alteration, it may be amenable to nonsense read-through therapy that is currently available or in clinical trial; This variant is associated with the following publications: (PMID: 28859693) |
Labcorp Genetics |
RCV000845039 | SCV003444449 | pathogenic | Duchenne muscular dystrophy | 2023-07-30 | 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: 620196). This premature translational stop signal has been observed in individual(s) with Duchenne muscular dystrophy (PMID: 28859693). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Trp1694*) in the DMD gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DMD are known to be pathogenic (PMID: 16770791, 25007885). |
Genome |
RCV000845039 | SCV000986876 | not provided | Duchenne muscular dystrophy | no assertion provided | phenotyping only | Variant interpretted as pathogenic and reported on 07/03/2018 by GTR ID 26957. GenomeConnect assertions are reported exactly as they appear on the patient-provided report from the testing laboratory. GenomeConnect staff make no attempt to reinterpret the clinical significance of the variant. |