Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000673274 | SCV000798457 | likely pathogenic | Sjögren-Larsson syndrome | 2018-03-12 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001385894 | SCV001585910 | pathogenic | not provided | 2023-03-04 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Val327*) in the ALDH3A2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ALDH3A2 are known to be pathogenic (PMID: 10577908, 10854114). This variant is present in population databases (rs779956047, gnomAD 0.01%). This variant has not been reported in the literature in individuals affected with ALDH3A2-related conditions. ClinVar contains an entry for this variant (Variation ID: 557168). For these reasons, this variant has been classified as Pathogenic. |
DASA | RCV000673274 | SCV002097290 | pathogenic | Sjögren-Larsson syndrome | 2022-02-14 | criteria provided, single submitter | clinical testing | The c.979del;p.(Val327*) is a null frameshift variant in the ALDH3A2 gene and predicts alteration of the nonsense-mediate decay - NMD is present in a relevant exon to the transcript -PVS1. This sequence change has been observed in affected individual(s) and ClinVar contains an entry for this variant (Clinvar ID: 557168) - PS4_supporting. This variant is not present in population databases (rs779956047, gnomAD; ABraOM no frequency - http://abraom.ib.usp.br/) - PM2. In summary, the currently available evidence indicates that the variant is pathogenic. |