Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Centre for Mendelian Genomics, |
RCV001198540 | SCV001369518 | likely pathogenic | Arrhythmogenic right ventricular dysplasia 10 | 2019-07-09 | criteria provided, single submitter | clinical testing | This variant was classified as: Likely pathogenic. The following ACMG criteria were applied in classifying this variant: PVS1,PM2. |
Labcorp Genetics |
RCV001198540 | SCV002131573 | pathogenic | Arrhythmogenic right ventricular dysplasia 10 | 2023-06-05 | 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: 931696). This premature translational stop signal has been observed in individual(s) with arrhythmogenic cardiomyopathy (PMID: 30847666). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Val271Ilefs*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). |
Gene |
RCV002284472 | SCV002574683 | likely pathogenic | not provided | 2022-09-16 | criteria provided, single submitter | clinical testing | Reported in a patient referred for arrhythmogenic right ventricular cardiomyopathy (ARVC) (van Lint et al., 2019); Not observed at significant frequency in large population cohorts (gnomAD); 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; This variant is associated with the following publications: (PMID: 30847666) |