Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV003877644 | SCV004684708 | pathogenic | Deficiency of ferroxidase | 2023-10-23 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu905*) in the CP gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CP are known to be pathogenic (PMID: 16629161). This variant is present in population databases (rs762368526, gnomAD 0.003%). This variant has not been reported in the literature in individuals affected with CP-related conditions. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004747403 | SCV005359874 | pathogenic | CP-related disorder | 2024-04-10 | no assertion criteria provided | clinical testing | The CP c.2712delC variant is predicted to result in premature protein termination (p.Leu905*). To our knowledge, this variant has not been reported in the literature. This variant is reported in just one allele of ~251,000 in gnomAD, indicating it is rare. Premature termination variants in CP are expected to be pathogenic, and nearby examples have been associated with disease (p.Arg901*, Takeuchi et al. 2002. PubMed ID: 11909923). Taken together, this variant is interpreted as pathogenic. |