Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Al Jalila Children’s Genomics Center, |
RCV002508873 | SCV002818148 | pathogenic | not provided | 2022-12-17 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003598143 | SCV004381494 | pathogenic | Transcobalamin II deficiency | 2023-01-16 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 1810225). For these reasons, this variant has been classified as Pathogenic. This variant disrupts a region of the TCN2 protein in which other variant(s) (p.Arg399*) have been determined to be pathogenic (PMID: 18956254, 31666257). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. This variant has not been reported in the literature in individuals affected with TCN2-related conditions. This variant is present in population databases (rs747615809, gnomAD 0.006%). This sequence change creates a premature translational stop signal (p.Leu376Phefs*36) in the TCN2 gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 52 amino acid(s) of the TCN2 protein. |
Centre for Inherited Metabolic Diseases, |
RCV003598143 | SCV005088244 | pathogenic | Transcobalamin II deficiency | 2024-07-23 | criteria provided, single submitter | clinical testing | The variant is a null variant causing frameshift (PVS1 - strong). This and other similar null variants have been reported to be causative (PM1, PMID:36703223, 20352340). The variant is rare in the healthy population (PM2-supporting). The clinical test in combination with phenotye allows for use of PP4 - strong (based on Biesecker et al. 2024 ClinGen guidance for use of the PP1/BS4 co-segregation and PP4 phenotype specificity criteria, PMID: 38103548). |