Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000187185 | SCV000240765 | likely pathogenic | not provided | 2021-09-29 | criteria provided, single submitter | clinical testing | 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 (Lek et al., 2016); Has not been previously published as pathogenic or benign to our knowledge |
Labcorp Genetics |
RCV000541323 | SCV000645078 | pathogenic | Cortical dysplasia-focal epilepsy syndrome | 2024-07-06 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg483*) in the CNTNAP2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CNTNAP2 are known to be pathogenic (PMID: 19896112, 21827697, 25045150, 26843181, 27439707). This variant is present in population databases (rs752550849, gnomAD 0.009%). This variant has not been reported in the literature in individuals affected with CNTNAP2-related conditions. ClinVar contains an entry for this variant (Variation ID: 205244). For these reasons, this variant has been classified as Pathogenic. |
Seattle Children's Hospital Molecular Genetics Laboratory, |
RCV002221212 | SCV002498592 | pathogenic | See cases | 2021-01-08 | criteria provided, single submitter | clinical testing | This variant is predicted to create a premature termination codon at protein position 483 and result in a loss of protein function. This variant has not been reported in the medical literature but loss-of-function variants in CNTNAP2 are known to be pathogenic. This is a rare variant in large population studies (3 of 251,318 alleles; Genome Aggregation Database v2.1.1). |