Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002819939 | SCV003199818 | pathogenic | Metachromatic leukodystrophy | 2022-05-28 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant disrupts a region of the ARSA protein in which other variant(s) (p.Cys491Gly) have been determined to be pathogenic (PMID: 15026521; Invitae). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. This variant has not been reported in the literature in individuals affected with ARSA-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Gln467*) in the ARSA gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 43 amino acid(s) of the ARSA protein. |
Prevention |
RCV003418614 | SCV004112843 | likely pathogenic | ARSA-related disorder | 2022-11-17 | criteria provided, single submitter | clinical testing | The ARSA c.1399C>T variant is predicted to result in premature protein termination (p.Gln467*). 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. Nonsense variants in ARSA are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Genome |
RCV002819939 | SCV006076312 | not provided | Metachromatic leukodystrophy | no assertion provided | phenotyping only | Variant classified as Pathogenic and reported on 06-01-2022 by Invitae. GenomeConnect-GM1 assertions are reported exactly as they appear on the patient-provided report from the testing laboratory. Registry team members make no attempt to reinterpret the clinical significance of the variant. Phenotypic details are available under supporting information. |