Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000726901 | SCV000703986 | pathogenic | not provided | 2016-12-12 | criteria provided, single submitter | clinical testing | |
Counsyl | RCV000592363 | SCV000793961 | likely pathogenic | Cohen syndrome | 2017-09-05 | criteria provided, single submitter | clinical testing | |
Invitae | RCV000592363 | SCV002151405 | pathogenic | Cohen syndrome | 2023-09-01 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Ile3284Asnfs*10) 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 not present in population databases (gnomAD no frequency). 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: 498787). For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV004024750 | SCV004980476 | pathogenic | Inborn genetic diseases | 2023-10-25 | criteria provided, single submitter | clinical testing | The c.9850dupA (p.I3284Nfs*10) alteration, located in exon 54 (coding exon 53) of the VPS13B gene, consists of a duplication of A at position 9850, causing a translational frameshift with a predicted alternate stop codon after 10 amino acids. This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. This variant was not reported in population-based cohorts in the Genome Aggregation Database (gnomAD). Based on the available evidence, this alteration is classified as pathogenic. |