Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Baylor Genetics | RCV001336527 | SCV001529929 | pathogenic | Sterol carrier protein 2 deficiency | 2018-05-07 | criteria provided, single submitter | clinical testing | This variant was determined to be pathogenic according to ACMG Guidelines, 2015 [PMID:25741868]. |
Labcorp Genetics |
RCV001871890 | SCV002229086 | pathogenic | not provided | 2024-11-11 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln371*) in the SCP2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SCP2 are known to be pathogenic (PMID: 16685654, 26497993). This variant is present in population databases (rs369561869, gnomAD 0.003%). This variant has not been reported in the literature in individuals affected with SCP2-related conditions. ClinVar contains an entry for this variant (Variation ID: 1033966). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004731130 | SCV005340285 | pathogenic | SCP2-related disorder | 2024-04-22 | no assertion criteria provided | clinical testing | The SCP2 c.1111C>T variant is predicted to result in premature protein termination (p.Gln371*). This variant has been reported in an individual with recurrent seizures (Nangia et al. 2022. PubMed ID: 36588923). This variant is reported in 0.0026% of alleles in individuals of European (non-Finnish) descent in gnomAD. Nonsense variants in SCP2 are expected to be pathogenic. This variant is interpreted as pathogenic. |