Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
ARUP Laboratories, |
RCV001812431 | SCV001471886 | pathogenic | not provided | 2020-03-23 | criteria provided, single submitter | clinical testing | The G6PD c.1376delG; p.Arg459fs variant, to our knowledge, is not reported in the medical literature or gene specific databases. This variant is also absent from general population databases (Exome Variant Server, Genome Aggregation Database), indicating it is not a common polymorphism. This variant causes a frameshift by deleting a single nucleotide, so it is predicted to result in a truncated protein or mRNA subject to nonsense-mediated decay. Large insertions/deletions, frameshift, and nonsense variants are not described in males for G6PD, consistent with the notion that a total lack of G6PD activity would be lethal (Vulliamy 1993). Therefore, the c.1376delG; p.Arg459fs variant is considered to be pathogenic. REFERENCES Vulliamy T et al. Variants of glucose-6-phosphate dehydrogenase are due to missense mutations spread throughout the coding region of the gene. Hum Mutat. 1993;2(3):159-67. |
Dunham Lab, |
RCV002305589 | SCV002599393 | pathogenic | Anemia, nonspherocytic hemolytic, due to G6PD deficiency | 2022-08-12 | criteria provided, single submitter | curation | Leads to frameshift that introduces a stop codon at residue 495 (PVS1). Not found in gnomAD (PM2). Reported as pathogenic by ARUP Laboratories (PP5). Post_P 0.997 (odds of pathogenicity 3152, Prior_P 0.1). |