Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001204375 | SCV001375580 | pathogenic | Perlman syndrome | 2023-09-08 | 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: 935724). This variant has not been reported in the literature in individuals affected with DIS3L2-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Cys216Alafs*122) in the DIS3L2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DIS3L2 are known to be pathogenic (PMID: 22306653, 28328139). |
Prevention |
RCV003398929 | SCV004110407 | likely pathogenic | DIS3L2-related disorder | 2023-03-02 | criteria provided, single submitter | clinical testing | The DIS3L2 c.645delC variant is predicted to result in a frameshift and premature protein termination (p.Cys216Alafs*122). To our knowledge, this variant has not been reported in the literature or in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Frameshift variants in DIS3L2 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Baylor Genetics | RCV001204375 | SCV004193943 | likely pathogenic | Perlman syndrome | 2023-03-30 | criteria provided, single submitter | clinical testing |