Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008103 | SCV001167852 | pathogenic | not provided | 2021-04-19 | criteria provided, single submitter | clinical testing | Frameshift 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: 23380217, 29419892, 33225392, 33290277) |
Labcorp Genetics |
RCV005093047 | SCV002235789 | pathogenic | not provided | 2023-11-06 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu284Valfs*10) in the DOCK8 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in DOCK8 are known to be pathogenic (PMID: 14722525, 19776401). This variant is present in population databases (rs762990689, gnomAD 0.003%). This premature translational stop signal has been observed in individual(s) with DOCK8 deficiency (PMID: 23380217). This variant is also known as c.850_851delCT (p.L284fsX293). ClinVar contains an entry for this variant (Variation ID: 817037). For these reasons, this variant has been classified as Pathogenic. |
OMIM | RCV001784550 | SCV002584914 | pathogenic | Combined immunodeficiency due to DOCK8 deficiency | 2023-10-05 | no assertion criteria provided | literature only |