Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000668515 | SCV000793133 | uncertain significance | Cohen syndrome | 2017-07-28 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000668515 | SCV001592713 | pathogenic | Cohen syndrome | 2023-11-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln1396*) 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 (rs559590419, gnomAD 0.01%). 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: 553132). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Neuberg Centre For Genomic Medicine, |
RCV000668515 | SCV002073145 | likely pathogenic | Cohen syndrome | criteria provided, single submitter | clinical testing | The stop gained p.Q1396* in VPS13B (NM_017890.5) has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. The p.Q1396* variant is observed in 2/30,612 (0.0065%) alleles from individuals of South Asian background in gnomAD Exomes and in 1/978 (0.1022%) alleles from individuals of South Asian background in 1000 Genomes. This variant is predicted to cause loss of normal protein function through protein truncation. Loss of function variants have been reported previously to be disease causing. For these reasons, this variant has been classified as Likely Pathogenic. |