Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008083 | SCV001167824 | pathogenic | not provided | 2022-06-30 | criteria provided, single submitter | clinical testing | 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 significant frequency in large population cohorts (gnomAD); Has not been previously published as pathogenic or benign to our knowledge |
Labcorp Genetics |
RCV001381140 | SCV001579393 | pathogenic | Arrhythmogenic cardiomyopathy with wooly hair and keratoderma; Arrhythmogenic right ventricular dysplasia 8 | 2020-10-08 | criteria provided, single submitter | clinical testing | Loss-of-function variants in DSP are known to be pathogenic (PMID: 20716751, 24503780, 25227139). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site, but this prediction has not been confirmed by published transcriptional studies. This variant has not been reported in the literature in individuals with DSP-related conditions. ClinVar contains an entry for this variant (Variation ID: 817029). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Leu1619Trpfs*26) in the DSP gene. It is expected to result in an absent or disrupted protein product. For these reasons, this variant has been classified as Pathogenic. |