Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001386109 | SCV001586216 | pathogenic | Werner syndrome | 2025-01-17 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln962*) in the WRN gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in WRN are known to be pathogenic (PMID: 16673358). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with Werner syndrome (PMID: 16673358, 29753700). ClinVar contains an entry for this variant (Variation ID: 1073193). For these reasons, this variant has been classified as Pathogenic. |
Baylor Genetics | RCV001386109 | SCV004208895 | pathogenic | Werner syndrome | 2023-11-12 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV001386109 | SCV005423340 | pathogenic | Werner syndrome | 2024-10-14 | criteria provided, single submitter | clinical testing | Variant summary: WRN c.2884C>T (p.Gln962X) results in a premature termination codon, predicted to cause absence of the protein due to nonsense mediated decay, which is a commonly known mechanism for disease. The variant was absent in 251266 control chromosomes (gnomAD). c.2884C>T has been reported in the literature in an individual(s) affected with Werner Syndrome (Huang_2006). The following publication has been ascertained in the context of this evaluation (PMID: 16673358). ClinVar contains an entry for this variant (Variation ID: 1073193). Based on the evidence outlined above, the variant was classified as pathogenic. |