Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003063385 | SCV003455584 | pathogenic | Glycogen storage disease, type VI | 2024-09-09 | criteria provided, single submitter | clinical testing | This variant results in the deletion of part of exon 16 of the PYGL gene. It is expected to disrupt RNA splicing. Variants that disrupt the donor or acceptor splice site typically lead to a loss of protein function (PMID: 16199547), and loss-of-function variants in PYGL are known to be pathogenic (PMID: 9536091, 21646031). Information on the frequency of this variant in the gnomAD database is not available, as this variant may be reported differently in the database. This variant has been observed in individuals with clinical features of glycogen storage disease (PMID: 17705025; internal data). This variant is also known as c.1964_1969inv6;c.1969+1_+4delGTAC. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003404048 | SCV004104256 | pathogenic | PYGL-related disorder | 2023-03-03 | criteria provided, single submitter | clinical testing | The PYGL c.1964_1969+4delinsGAAAAA variant is predicted to result in an in-frame deletion and insertion. This variant is predicted to abolish a canonical splice site. This variant was reported in the compound heterozygous state in an individual with glycogen storage disease 6 (Beauchamp et al. 2007. PubMed ID: 17705025). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. This variant is interpreted as pathogenic. |