Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Genetics and Molecular Pathology, |
RCV002272801 | SCV002557026 | pathogenic | Maturity-onset diabetes of the young type 2 | 2020-11-05 | criteria provided, single submitter | clinical testing | |
Geisinger Clinic, |
RCV002272801 | SCV002562186 | pathogenic | Maturity-onset diabetes of the young type 2 | 2022-08-02 | criteria provided, single submitter | research | PVS1, PM2, PS4_Supporting, PP1_Strong, PP4 |
Laboratory for Molecular Medicine, |
RCV004017916 | SCV004848492 | likely pathogenic | Maturity onset diabetes mellitus in young | 2020-11-06 | criteria provided, single submitter | clinical testing | The (c.638dupA) p.Tyr213Ter variant in GCK has not been reported in individuals with maturity-onset diabetes of the young (MODY) and was absent from large population studies. This single base duplication variant leads to a premature termination codon at position 213, which is predicted to lead to a truncated or absent protein. Heterozygous loss of function of the GCK gene is an established disease mechanism in maturity-onset diabetes of the young. In summary, although additional studies are required to fully establish its clinical significance, this variant is likely pathogenic for autosomal dominant MODY. ACMG/AMP Criteria applied: PVS1, PM2. |