Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ambry Genetics | RCV002355448 | SCV002623585 | pathogenic | Maturity onset diabetes mellitus in young | 2015-05-07 | criteria provided, single submitter | clinical testing | The c.1156delC (p.L386Wfs*16) pathogenic mutation, located in coding exon 9 of the GCK gene, results from a deletion of one nucleotide at position 1156, causing a translational frameshift with a predicted alternate stop codon. Since frameshifts are typically deleterious in nature, this alteration is interpreted as a disease-causing mutation (ACMG Recommendations for Standards for Interpretation and Reporting of Sequence Variations. Revision 2007. Genet Med. 2008;10:294). |
Labcorp Genetics |
RCV003094397 | SCV003315010 | pathogenic | not provided | 2023-10-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu386Trpfs*16) in the GCK gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in GCK are known to be pathogenic (PMID: 7553875, 9867845, 14578306, 24323243, 25015100). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with autosomal dominant GCK-related conditions (PMID: 32533152). ClinVar contains an entry for this variant (Variation ID: 1735443). For these reasons, this variant has been classified as Pathogenic. |