Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
3billion, |
RCV002251200 | SCV002521712 | pathogenic | Glycogen storage disease IXc | 2022-05-22 | criteria provided, single submitter | clinical testing | The variant is not observed in the gnomAD v2.1.1 dataset. 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. Therefore, this variant is classified as pathogenic according to the recommendation of ACMG/AMP guideline. |
Labcorp Genetics |
RCV002251200 | SCV005737948 | likely pathogenic | Glycogen storage disease IXc | 2024-04-06 | criteria provided, single submitter | clinical testing | This variant results in the deletion of part of exon 8 (c.800_801+34del) of the PHKG2 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 PHKG2 are known to be pathogenic (PMID: 8896567, 17689125, 21646031). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with PHKG2-related conditions. ClinVar contains an entry for this variant (Variation ID: 1687518). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |