Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV000519932 | SCV000617557 | pathogenic | not provided | 2018-05-18 | criteria provided, single submitter | clinical testing | The c.580-1 G>A splice site variant in the GCK gene has been previously reported in association with MODY (Toaima et al., 2005; Gozlan et al., 2012). This variant destroys the canonical splice acceptor site in intron 5, and is expected to cause abnormal gene splicing (Toaima et al., 2005). The variant is not observed in large population cohorts (Lek et al., 2016; 1000 Genomes Consortium et al., 2015; Exome Variant Server). In summary, we consider this variant to be pathogenic. |
Geisinger Clinic, |
RCV002285354 | SCV002562185 | pathogenic | Maturity-onset diabetes of the young type 2 | 2022-08-02 | criteria provided, single submitter | research | PVS1, PM2, PP3, PS4_supporting, PP4 |
3billion | RCV002285354 | SCV005906028 | pathogenic | Maturity-onset diabetes of the young type 2 | 2023-09-15 | criteria provided, single submitter | clinical testing | The variant is not observed in the gnomAD v2.1.1 dataset. Predicted Consequence/Location: Canonical splice site: predicted to alter splicing and result in a loss or disruption of normal protein function. Multiple pathogenic loss-of-function variants are reported downstream of the variant. The variant has been reported at least twice as pathogenic without evidence for the classification (ClinVar ID: VCV000449414 /PMID: 15841481). Therefore, this variant is classified as Pathogenic according to the recommendation of ACMG/AMP guideline. |