Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001934875 | SCV002130979 | pathogenic | Walker-Warburg congenital muscular dystrophy | 2021-08-16 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Phe61Ilefs*16) in the FKTN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FKTN are known to be pathogenic (PMID: 17044012, 17878207, 18752264). For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with FKTN-related conditions. This variant is not present in population databases (ExAC no frequency). |
Ambry Genetics | RCV004996048 | SCV005581300 | pathogenic | Cardiovascular phenotype | 2024-09-18 | criteria provided, single submitter | clinical testing | The c.180dupA pathogenic mutation, located in coding exon 3 of the FKTN gene, results from a duplication of A at nucleotide position 180, causing a translational frameshift with a predicted alternate stop codon (p.F61Ifs*16). This variant is considered to be rare based on population cohorts in the Genome Aggregation Database (gnomAD). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |