Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000290082 | SCV000330130 | pathogenic | not provided | 2024-05-10 | criteria provided, single submitter | clinical testing | Observed in patients with ARVC referred for genetic testing at GeneDx and in the published literature (PMID: 27532257); Frameshift 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 at a significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 31447099, 31402444, 33087929, 27532257) |
Labcorp Genetics |
RCV000813935 | SCV000954319 | pathogenic | Arrhythmogenic right ventricular dysplasia 10 | 2022-10-17 | 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: 280230). This premature translational stop signal has been observed in individual(s) with arrhythmogenic right ventricular cardiomyopathy (PMID: 27532257). This variant is present in population databases (rs781532110, gnomAD 0.008%). This sequence change creates a premature translational stop signal (p.Gly166Trpfs*4) in the DSG2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DSG2 are known to be pathogenic (PMID: 17105751, 31386562). |
Fulgent Genetics, |
RCV002503975 | SCV002813246 | pathogenic | Arrhythmogenic right ventricular dysplasia 10; Dilated cardiomyopathy 1BB | 2021-11-08 | criteria provided, single submitter | clinical testing |