Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clinical Genetics and Genomics, |
RCV001269547 | SCV001449605 | pathogenic | not provided | 2015-12-15 | criteria provided, single submitter | clinical testing | |
Gene |
RCV001269547 | SCV003798890 | uncertain significance | not provided | 2023-01-31 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Has not been previously published as pathogenic or benign to our knowledge |
Neuberg Centre For Genomic Medicine, |
RCV004584871 | SCV005073903 | likely pathogenic | ALG3-congenital disorder of glycosylation | criteria provided, single submitter | clinical testing | The stop gained c.349C>T (p.Arg117Ter) variant in the ALG3 gene has not been reported previously as a pathogenic variant nor as a benign variant, to our knowledge. This variant is reported with the allele frequency (0.004%) in the gnomAD Exomes. It is submitted to ClinVar as Pathogenic/ Uncertain Significance. However, no details are available for independent assessment. This variant is predicted to cause loss of normal protein function either through protein truncation or nonsense-mediated mRNA decay. Loss of function variants have been previously reported to be disease causing. The nucleotide change c.349C>T in ALG3 is predicted as conserved by GERP++ and PhyloP across 100 vertebrates. Further studies are required to prove the pathogenicity of the variant. For these reasons, this variant has been classified as Likely Pathogenic. |