Total submissions: 11
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000169573 | SCV000221073 | likely pathogenic | Glycogen storage disease type III | 2015-01-23 | criteria provided, single submitter | literature only | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000001152 | SCV000697534 | pathogenic | Glycogen storage disease IIIa | 2017-01-06 | criteria provided, single submitter | clinical testing | Variant summary: The AGL c.4529dupA (p.Tyr1510X) variant results in a premature termination codon, predicted to cause a truncated or absent AGL protein due to nonsense mediated decay, which are commonly known mechanisms for disease. The variant of interest was observed in the large, broad control population, ExAC, with an allele frequency of 2/121034 (1/60517), which does not exceed the estimated maximal expected allele frequency for a pathogenic AGL variant of 1/438. Multiple publications have cited the variant in affected individuals, who were homozygous and compound heterozygous. In addition, multiple clinical diagnostic laboratories/reputable databases classified this variant as likely pathogenic/pathogenic. Taken together, this variant is classified as pathogenic. |
Labcorp Genetics |
RCV000169573 | SCV000752145 | pathogenic | Glycogen storage disease type III | 2024-12-18 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr1510*) in the AGL gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 23 amino acid(s) of the AGL protein. This variant is present in population databases (rs756759628, gnomAD 0.004%). This premature translational stop signal has been observed in individuals with glycogen storage disease type III (PMID: 8990006, 20071996, 20490926, 23430490). ClinVar contains an entry for this variant (Variation ID: 1094). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Ambry Genetics | RCV001265666 | SCV001443833 | pathogenic | Inborn genetic diseases | 2016-03-01 | criteria provided, single submitter | clinical testing | |
Genome- |
RCV000169573 | SCV002055514 | pathogenic | Glycogen storage disease type III | 2021-07-15 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV000169573 | SCV002811460 | likely pathogenic | Glycogen storage disease type III | 2021-07-12 | criteria provided, single submitter | clinical testing | |
Revvity Omics, |
RCV000169573 | SCV003816708 | pathogenic | Glycogen storage disease type III | 2022-01-13 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000169573 | SCV004212970 | pathogenic | Glycogen storage disease type III | 2024-01-24 | criteria provided, single submitter | clinical testing | |
OMIM | RCV000001152 | SCV000021302 | pathogenic | Glycogen storage disease IIIa | 1997-01-01 | no assertion criteria provided | literature only | |
Natera, |
RCV000169573 | SCV001460668 | pathogenic | Glycogen storage disease type III | 2020-09-16 | no assertion criteria provided | clinical testing | |
Gene |
RCV000169573 | SCV002072438 | not provided | Glycogen storage disease type III | no assertion provided | literature only | Associated with more severe phenotype |