Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Laboratory for Molecular Medicine, |
RCV000616190 | SCV000712848 | uncertain significance | not specified | 2017-01-17 | criteria provided, single submitter | clinical testing | The p.Arg268X variant in TSPEAR has not been previously reported in individuals with hearing loss, but has been identified in 1/66396 of European chromosomes by the Exome Aggregation Consortium (ExAC, http://exac.broadinstitute.org; dbSNP r s782471965). Although this variant has been seen in the general population, its frequency is not high enough to rule out a pathogenic role. This nonsense varian t leads to a premature termination codon at position 268, which is predicted to lead to a truncated or absent protein. However, there is only moderate evidence to support an association of TSPEAR with autosomal recessive nonsyndromic hearin g loss. In summary, the clinical significance of the p.Arg268X variant is uncert ain. |
Labcorp Genetics |
RCV003767454 | SCV004624791 | pathogenic | not provided | 2023-06-20 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 505557). For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with TSPEAR-related conditions. This sequence change creates a premature translational stop signal (p.Arg268*) in the TSPEAR gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in TSPEAR are known to be pathogenic (PMID: 34042254). This variant is present in population databases (rs782471965, gnomAD 0.0009%). |