Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001229117 | SCV001401554 | pathogenic | ALG8 congenital disorder of glycosylation | 2022-02-03 | 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: 956334). This variant has not been reported in the literature in individuals affected with ALG8-related conditions. This variant is present in population databases (rs777686455, gnomAD 0.02%). This sequence change creates a premature translational stop signal (p.Val328Serfs*28) in the ALG8 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ALG8 are known to be pathogenic (PMID: 19862844). |
Fulgent Genetics, |
RCV002497778 | SCV002810047 | likely pathogenic | ALG8 congenital disorder of glycosylation; Polycystic liver disease 3 with or without kidney cysts | 2022-01-25 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV004538480 | SCV004105966 | likely pathogenic | ALG8-related disorder | 2023-07-19 | criteria provided, single submitter | clinical testing | The ALG8 c.981dupA variant is predicted to result in a frameshift and premature protein termination (p.Val328Serfs*28). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.018% of alleles in individuals of European (Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/11-77820544-C-CT). Frameshift variants in ALG8 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Laboratory of Gastroenterology and Hepatology, |
RCV003448985 | SCV003934878 | pathogenic | Autosomal dominant polycystic liver disease | 2021-06-08 | no assertion criteria provided | research |