Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Center for Genomic Medicine, |
RCV000171184 | SCV000221381 | likely pathogenic | not provided | criteria provided, single submitter | research | ||
Invitae | RCV000171184 | SCV002247295 | pathogenic | not provided | 2022-03-09 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg238*) in the PDE6C gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in PDE6C are known to be pathogenic (PMID: 19887631, 23776498, 26103963, 30080950). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 191009). This premature translational stop signal has been observed in individual(s) with achromatopsia and/or retinal dystrophy (PMID: 27124789). This variant is present in population databases (rs762426409, gnomAD 0.006%). |
3billion | RCV001781531 | SCV002521750 | pathogenic | Cone dystrophy 4 | 2022-05-22 | criteria provided, single submitter | clinical testing | The variant is observed at an extremely low frequency in the gnomAD v2.1.1 dataset (total allele frequency: <0.001%). Stop-gained (nonsense): predicted to result in a loss or disruption of normal protein function through nonsense-mediated decay (NMD) or protein truncation. Multiple pathogenic variants are reported downstream of the variant. The variant has been reported to be associated with PDE6C related disorder (ClinVar ID: VCV000191009 / PMID: 27124789). Therefore, this variant is classified as pathogenic according to the recommendation of ACMG/AMP guideline. |