Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000169432 | SCV000220845 | likely pathogenic | Cohen syndrome | 2014-10-28 | criteria provided, single submitter | literature only | |
Labcorp Genetics |
RCV000169432 | SCV002242790 | pathogenic | Cohen syndrome | 2022-11-15 | 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: 68086). This premature translational stop signal has been observed in individual(s) with clinical features of Cohen syndrome (PMID: 16648375). This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Trp1641*) 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). |
Gene |
RCV000058896 | SCV002526256 | pathogenic | not provided | 2022-06-03 | criteria provided, single submitter | clinical testing | Observed along with a second nonsense variant in the VPS13B gene in multiple patients from one family with Cohen syndrome; however, segregation information was not provided (Seifert et al., 2006); Nonsense 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 significant frequency in large population cohorts (gnomAD); This variant is associated with the following publications: (PMID: 25525159, 21865173, 20461111, 15141358, 16648375) |
SNPedia | RCV000058896 | SCV000090417 | pathogenic | not provided | no assertion criteria provided | not provided | Converted during submission to Pathogenic. |