Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000413946 | SCV000491590 | pathogenic | not provided | 2023-02-06 | criteria provided, single submitter | clinical testing | Identified in the compound heterozygous state with another SNX14 variant in a patient with early-onset epileptic encephalopathy in published literature (Tsuchida et al., 2018); Nonsense 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); This variant is associated with the following publications: (PMID: 28940419, 36305856) |
Centogene AG - |
RCV001808789 | SCV002059453 | pathogenic | Autosomal recessive spinocerebellar ataxia 20 | 2019-03-06 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000413946 | SCV003279508 | pathogenic | not provided | 2017-11-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Glu370*) in the SNX14 gene. It is expected to result in an absent or disrupted protein product. This variant is present in population databases (rs201128942, ExAC 0.005%). This variant has not been reported in the literature in individuals with SNX14-related disease. ClinVar contains an entry for this variant (Variation ID: 373031). Loss-of-function variants in SNX14 are known to be pathogenic (PMID: 25439728, 25848753). For these reasons, this variant has been classified as Pathogenic. |
Genome |
RCV001808789 | SCV002074902 | not provided | Autosomal recessive spinocerebellar ataxia 20 | no assertion provided | phenotyping only | Variant interpreted as Pathogenic and reported on 11-01-2016 by Lab or GTR ID 26957. GenomeConnect assertions are reported exactly as they appear on the patient-provided report from the testing laboratory. GenomeConnect staff make no attempt to reinterpret the clinical significance of the variant. |