Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetic Services Laboratory, |
RCV000409909 | SCV000597922 | pathogenic | Cohen syndrome | 2016-01-20 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001561612 | SCV001784241 | likely pathogenic | not provided | 2019-08-14 | 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); Has not been previously published as pathogenic or benign to our knowledge |
Fulgent Genetics, |
RCV000409909 | SCV002775340 | pathogenic | Cohen syndrome | 2021-09-01 | criteria provided, single submitter | clinical testing | |
Invitae | RCV000409909 | SCV002989117 | pathogenic | Cohen syndrome | 2023-10-07 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg3865Serfs*13) in the VPS13B gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in VPS13B are known to be pathogenic (PMID: 15141358, 16648375, 20461111). This variant is present in population databases (rs747217399, gnomAD 0.002%). This variant has not been reported in the literature in individuals affected with VPS13B-related conditions. ClinVar contains an entry for this variant (Variation ID: 371090). For these reasons, this variant has been classified as Pathogenic. |
Counsyl | RCV000409909 | SCV000486565 | likely pathogenic | Cohen syndrome | 2016-06-24 | no assertion criteria provided | clinical testing | |
Natera, |
RCV000409909 | SCV002082801 | likely pathogenic | Cohen syndrome | 2020-02-04 | no assertion criteria provided | clinical testing |