Total submissions: 9
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000080803 | SCV000112705 | pathogenic | not provided | 2017-12-14 | criteria provided, single submitter | clinical testing | |
Athena Diagnostics | RCV000179204 | SCV000255754 | pathogenic | Duchenne muscular dystrophy | 2013-01-08 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000179204 | SCV000550335 | pathogenic | Duchenne muscular dystrophy | 2024-07-08 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg2870*) 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). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individuals with Duchenne muscular dystrophy (PMID: 11524473, 16834926, 19783145, 20098710, 20485447, 21396098, 23588064). ClinVar contains an entry for this variant (Variation ID: 94810). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV000080803 | SCV001764249 | pathogenic | not provided | 2017-11-20 | criteria provided, single submitter | clinical testing | 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: 27593222, 26968818, 19783145, 11524473, 25525159, 23588064, 20485447, 17253928, 12632325) |
Revvity Omics, |
RCV000080803 | SCV002022894 | pathogenic | not provided | 2023-01-17 | criteria provided, single submitter | clinical testing | |
Laboratory of Medical Genetics, |
RCV000179204 | SCV002769625 | pathogenic | Duchenne muscular dystrophy | 2022-12-16 | criteria provided, single submitter | clinical testing | PVS1, PM2, PP5 |
Prevention |
RCV004528291 | SCV004110988 | pathogenic | DMD-related disorder | 2023-03-03 | criteria provided, single submitter | clinical testing | The DMD c.8608C>T variant is predicted to result in premature protein termination (p.Arg2870*). This variant has been reported in many individuals with Duchenne muscular dystrophy (reported as "8921C>T; R2905X" in Mendell et al. 2001. PubMed ID: 11524473; Cho et al. 2017. PubMed ID: 27593222; Table S3 in Fan et al. 2021. PubMed ID: 34006472). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Nonsense variants in DMD are expected to be pathogenic, and this variant has been classified as pathogenic by multiple independent submitters to the ClinVar database (https://www.ncbi.nlm.nih.gov/clinvar/variation/94810). This variant is interpreted as pathogenic. |
Beijing Key Laboratory for Genetic Research of Skeletal Deformity, |
RCV000179204 | SCV001482345 | pathogenic | Duchenne muscular dystrophy | 2019-05-31 | no assertion criteria provided | research | |
Natera, |
RCV001831875 | SCV002087660 | pathogenic | Becker muscular dystrophy; Duchenne muscular dystrophy; Cardiomyopathy; Dystrophin deficiency | 2020-05-15 | no assertion criteria provided | clinical testing |