Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001950939 | SCV002234359 | pathogenic | X-linked myopathy with postural muscle atrophy | 2022-03-08 | criteria provided, single submitter | clinical testing | For these reasons, this variant has been classified as Pathogenic. Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. This variant has not been reported in the literature in individuals affected with FHL1-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Tyr176*) 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). |
ARUP Laboratories, |
RCV003741285 | SCV004564543 | likely pathogenic | Familial hemophagocytic lymphohistiocytosis type 1 | 2023-10-18 | criteria provided, single submitter | clinical testing | The FHL1 c.528C>G; p.Tyr176Ter variant, to our knowledge, is not reported in the medical literature but is reported in ClinVar (Variation ID: 1456031). This variant is also absent from the Genome Aggregation Database, indicating it is not a common polymorphism. This variant induces an early termination codon and is predicted to result in a truncated protein or mRNA subject to nonsense-mediated decay. Based on available information, this variant is considered to be likely pathogenic. |