Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001956073 | SCV002247047 | pathogenic | X-linked myopathy with postural muscle atrophy | 2021-08-29 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with FHL1-related conditions. This variant is not present in population databases (ExAC no frequency). This sequence change creates a premature translational stop signal (p.Phe80Leufs*72) in the FHL1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in FHL1 are known to be pathogenic (PMID: 18179888, 19687455, 19716112, 22523091, 24114807). |
Ambry Genetics | RCV002442948 | SCV002733738 | pathogenic | Cardiovascular phenotype | 2022-02-16 | criteria provided, single submitter | clinical testing | The c.240delT pathogenic mutation, located in coding exon 2 of the FHL1 gene, results from a deletion of one nucleotide at nucleotide position 240, causing a translational frameshift with a predicted alternate stop codon (p.F80Lfs*72). 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. |