Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001780646 | SCV002190522 | pathogenic | not provided | 2021-12-22 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Trp62*) in the ASAH1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ASAH1 are known to be pathogenic (PMID: 24164096, 24355074). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This variant has not been reported in the literature in individuals affected with ASAH1-related conditions. ClinVar contains an entry for this variant (Variation ID: 1323941). For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV002482308 | SCV002791708 | likely pathogenic | Spinal muscular atrophy-progressive myoclonic epilepsy syndrome; Farber lipogranulomatosis | 2021-09-14 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004738381 | SCV005363649 | likely pathogenic | ASAH1-related disorders | 2024-06-03 | no assertion criteria provided | clinical testing | The ASAH1 c.234G>A variant is predicted to result in premature protein termination (p.Trp78*). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.0018% of alleles in individuals of European (Non-Finnish) descent in gnomAD. Nonsense variants in ASAH1 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |