Total submissions: 8
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000078587 | SCV000230062 | likely pathogenic | not provided | 2013-08-30 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000078587 | SCV000617239 | pathogenic | not provided | 2022-07-01 | criteria provided, single submitter | clinical testing | Not observed at a significant frequency in large population cohorts (gnomAD); In silico analysis supports that this missense variant has a deleterious effect on protein structure/function; This variant is associated with the following publications: (PMID: 11058895, 9781052, 15771971, 9497260, 9425221, 9140401, 25497157, 25355454, 15844218, 34234304, 34480478) |
Labcorp Genetics |
RCV000178072 | SCV000938657 | pathogenic | PMM2-congenital disorder of glycosylation | 2024-01-24 | criteria provided, single submitter | clinical testing | This sequence change replaces alanine, which is neutral and non-polar, with valine, which is neutral and non-polar, at codon 108 of the PMM2 protein (p.Ala108Val). This variant is present in population databases (rs200503569, gnomAD 0.003%). This missense change has been observed in individual(s) with PMM2-related conditions (PMID: 9140401, 15844218, 25355454). In at least one individual the data is consistent with being in trans (on the opposite chromosome) from a pathogenic variant. ClinVar contains an entry for this variant (Variation ID: 92800). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) has been performed at Invitae for this missense variant, however the output from this modeling did not meet the statistical confidence thresholds required to predict the impact of this variant on PMM2 protein function. For these reasons, this variant has been classified as Pathogenic. |
Medical Cytogenetics and Molecular Genetics Laboratory, |
RCV001270234 | SCV001364365 | pathogenic | Premature ovarian failure | 2020-03-02 | criteria provided, single submitter | research | |
Molecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, |
RCV000178072 | SCV001519165 | pathogenic | PMM2-congenital disorder of glycosylation | 2021-01-04 | criteria provided, single submitter | research | |
Myriad Genetics, |
RCV000178072 | SCV002060161 | likely pathogenic | PMM2-congenital disorder of glycosylation | 2021-11-10 | criteria provided, single submitter | clinical testing | NM_000303.2(PMM2):c.323C>T(A108V) is a missense variant classified as likely pathogenic in the context of congenital disorder of glycosylation type Ia. A108V has been observed in cases with relevant disease (PMID: 32635232, Gurtunca_2013 _(no PMID; abstract), 25355454, 25497157, 15844218). Functional assessments of this variant are not available in the literature. A108V has been observed in population frequency databases (gnomAD: NFE 0.002%). In summary, NM_000303.2(PMM2):c.323C>T(A108V) is a missense variant that has been observed more frequently in cases with the relevant disease than in healthy populations. Please note: this variant was assessed in the context of healthy population screening. |
Fulgent Genetics, |
RCV000178072 | SCV002803300 | likely pathogenic | PMM2-congenital disorder of glycosylation | 2021-08-12 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000178072 | SCV004205264 | pathogenic | PMM2-congenital disorder of glycosylation | 2024-03-12 | criteria provided, single submitter | clinical testing |