Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000731858 | SCV000859714 | likely benign | not specified | 2018-03-01 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000903690 | SCV001048170 | likely benign | not provided | 2024-01-09 | criteria provided, single submitter | clinical testing | |
Mendelics | RCV000987376 | SCV001136659 | benign | Autosomal dominant optic atrophy classic form | 2023-08-22 | criteria provided, single submitter | clinical testing | |
Gene |
RCV000903690 | SCV001776758 | likely benign | not provided | 2021-06-22 | criteria provided, single submitter | clinical testing | In silico analysis, which includes protein predictors and evolutionary conservation, supports a deleterious effect; This variant is associated with the following publications: (PMID: 22707247, 21036400, 18783614, 16617242) |
Prevention |
RCV004737986 | SCV005364984 | uncertain significance | OPA1-related disorder | 2024-09-17 | no assertion criteria provided | clinical testing | The OPA1 c.239A>G variant is predicted to result in the amino acid substitution p.Tyr80Cys. This variant has been reported in two apparently unrelated patients with optic atrophy (Han et al., 2006. PubMed ID: 16617242; Yu-Wai-Man et al., 2010. PubMed ID: 21036400). However, no conclusive evidence of pathogenicity was provided. In addition, one of these patients harbored another variant of uncertain significance in OPA1 (Han et al. 2006. PubMed ID: 16617242). This variant is reported in 0.39% of alleles in individuals of African descent in gnomAD, which may be too common to be a primary cause of disease. Although we suspect that this variant may be benign, at this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |