Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000080405 | SCV000112307 | pathogenic | not provided | 2017-04-13 | criteria provided, single submitter | clinical testing | |
Centre for Mendelian Genomics, |
RCV001196295 | SCV001366875 | pathogenic | Dilated cardiomyopathy 3B | 2016-01-01 | criteria provided, single submitter | clinical testing | This variant was classified as: Pathogenic. This variant was detected in hemizygous state. |
Revvity Omics, |
RCV000080405 | SCV002022892 | pathogenic | not provided | 2020-04-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003512011 | SCV004299540 | pathogenic | Duchenne muscular dystrophy | 2023-10-04 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 69 of the DMD gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and 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). Disruption of this splice site has been observed in individual(s) with Duchenne muscular dystrophy (PMID: 7581396, 8589698, 19937601, 32194622). ClinVar contains an entry for this variant (Variation ID: 94422). Studies have shown that disruption of this splice site is associated with altered splicing resulting in multiple RNA products (PMID: 7581396, 8589698). For these reasons, this variant has been classified as Pathogenic. |