Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV000001217 | SCV000939194 | pathogenic | Glycogen storage disease, type VII | 2023-05-18 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 1158). This premature translational stop signal has been observed in individual(s) with glycogen storage disease type VII (PMID: 7479776). The frequency data for this variant in the population databases is considered unreliable, as metrics indicate poor data quality at this position in the gnomAD database. This sequence change creates a premature translational stop signal (p.Arg95*) in the PFKM gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PFKM are known to be pathogenic (PMID: 7825568, 8037209). For these reasons, this variant has been classified as Pathogenic. |
UNC Molecular Genetics Laboratory, |
RCV000001217 | SCV001251486 | likely pathogenic | Glycogen storage disease, type VII | criteria provided, single submitter | research | The PFKM c.496C>T (p.R166*) nonsense variant is predicted to result in an absent or aberrant protein. This variant was previously reported in the homozygous state in one mother and in her two daughters affected with glycogen storage disease type VII (PMID: 7479776). | |
Baylor Genetics | RCV000001217 | SCV004203955 | pathogenic | Glycogen storage disease, type VII | 2024-01-09 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000001217 | SCV000021367 | pathogenic | Glycogen storage disease, type VII | 1995-10-24 | no assertion criteria provided | literature only |