Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000760673 | SCV000890565 | pathogenic | not provided | 2019-10-09 | criteria provided, single submitter | clinical testing | 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 a significant frequency in large population cohorts (Lek et al., 2016); This variant is associated with the following publications: (PMID: 25412400, 28724398, 31054281, 31630094) |
Labcorp Genetics |
RCV001854999 | SCV002234978 | pathogenic | Alstrom syndrome | 2023-06-25 | 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: 264657). This premature translational stop signal has been observed in individual(s) with Alstrom syndrome (PMID: 28724398). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. It has also been observed to segregate with disease in related individuals. This variant is present in population databases (rs769219669, gnomAD 0.01%). This sequence change creates a premature translational stop signal (p.Ser1301*) in the ALMS1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ALMS1 are known to be pathogenic (PMID: 17594715). |