Total submissions: 3
| Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
|---|---|---|---|---|---|---|---|---|
| Gene |
RCV001008915 | SCV001168721 | pathogenic | not provided | 2019-10-23 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss-of-function is a known mechanism of disease; Not observed in large population cohorts (Lek et al., 2016); Has not been previously published as pathogenic or benign to our knowledge |
| Labcorp Genetics |
RCV005089392 | SCV005744341 | pathogenic | Tuberous sclerosis 2 | 2024-03-14 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Asp8Ilefs*4) in the TSC2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TSC2 are known to be pathogenic (PMID: 10205261, 17304050). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with TSC2-related conditions. ClinVar contains an entry for this variant (Variation ID: 49599). For these reasons, this variant has been classified as Pathogenic. |
| Tuberous sclerosis database |
RCV000042860 | SCV000066656 | not provided | Tuberous sclerosis syndrome | no assertion provided | curation |