Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000409691 | SCV000486267 | likely pathogenic | Cohen syndrome | 2016-04-28 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000598802 | SCV000710030 | pathogenic | not provided | 2020-10-23 | criteria provided, single submitter | clinical testing | Observed with another VPS13B variant on the opposite allele (in trans) in a patient with microcephaly and malformation of cortical development in published literature (Zillhardt et al., 2016); 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: 29149870, 26395554) |
Labcorp Genetics |
RCV000409691 | SCV002131466 | pathogenic | Cohen syndrome | 2023-12-09 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Met2124Valfs*44) 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 (rs748404277, gnomAD 0.002%). This premature translational stop signal has been observed in individual(s) with VPS13B-related conditions (PMID: 26395554, 29149870). This variant is also known as c.6295_6296delAT. ClinVar contains an entry for this variant (Variation ID: 242548). For these reasons, this variant has been classified as Pathogenic. |
NIHR Bioresource Rare Diseases, |
RCV000504997 | SCV000598902 | uncertain significance | Abnormality of the eye | 2015-01-01 | no assertion criteria provided | research |