Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Gene |
RCV001008881 | SCV001168687 | pathogenic | not provided | 2018-06-11 | criteria provided, single submitter | clinical testing | The c.5769dupT variant in the SPG11 gene causes a frameshift starting with codon Methionine 1924,changes this amino acid to a Tyrosine residue and creates a premature Stop codon at position 16 ofthe new reading frame, denoted p.Met1924TyrfsX16. This variant is predicted to cause loss of normalprotein function either through protein truncation or nonsense-mediated mRNA decay. Thec.5769dupT variant is not observed in large population cohorts (Lek et al., 2016). |
Labcorp Genetics |
RCV001860597 | SCV002242055 | pathogenic | Hereditary spastic paraplegia 11 | 2021-10-15 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Met1924Tyrfs*16) in the SPG11 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SPG11 are known to be pathogenic (PMID: 19105190, 20110243, 22154821, 26556829). This variant is not present in population databases (ExAC no frequency). This variant has not been reported in the literature in individuals affected with SPG11-related conditions. ClinVar contains an entry for this variant (Variation ID: 817675). For these reasons, this variant has been classified as Pathogenic. |
Genome- |
RCV001860597 | SCV002763793 | pathogenic | Hereditary spastic paraplegia 11 | criteria provided, single submitter | clinical testing |