Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001919773 | SCV002159566 | pathogenic | Nemaline myopathy 7 | 2021-08-02 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This premature translational stop signal has been observed in individual(s) with nemaline myopathy (PMID: 24610938). This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Lys34Glnfs*6) in the CFL2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in CFL2 are known to be pathogenic (PMID: 24610938, 27447704, 29457652). |
Prevention |
RCV003416556 | SCV004118393 | pathogenic | CFL2-related disorder | 2023-09-28 | criteria provided, single submitter | clinical testing | The CFL2 c.100_103delAAAG variant is predicted to result in a frameshift and premature protein termination (p.Lys34Glnfs*6). This variant has been reported in the homozygous state to be causative for autosomal recessive early-onset nemaline myopathy in a single patient (Ong et al. 2014. PubMed ID: 24610938). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Frameshift variants in CFL2 are expected to be pathogenic. This variant is interpreted as pathogenic. |