Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000665463 | SCV000789593 | likely pathogenic | PMM2-congenital disorder of glycosylation | 2017-02-07 | criteria provided, single submitter | clinical testing | |
Fulgent Genetics, |
RCV000665463 | SCV002789181 | likely pathogenic | PMM2-congenital disorder of glycosylation | 2021-12-28 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000665463 | SCV003498720 | pathogenic | PMM2-congenital disorder of glycosylation | 2023-12-26 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (Splice site) in the PMM2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PMM2 are known to be pathogenic (PMID: 19862844). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with PMM2-related conditions. This variant is also known as c.66+1del. ClinVar contains an entry for this variant (Variation ID: 550661). 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. |
Baylor Genetics | RCV000665463 | SCV004205294 | likely pathogenic | PMM2-congenital disorder of glycosylation | 2023-03-20 | criteria provided, single submitter | clinical testing |