Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ce |
RCV000722754 | SCV002545737 | likely pathogenic | not provided | 2022-04-01 | criteria provided, single submitter | clinical testing | SLX4: PVS1:Strong, PM2 |
Labcorp Genetics |
RCV002533067 | SCV003259058 | pathogenic | Fanconi anemia | 2023-04-03 | criteria provided, single submitter | clinical testing | ClinVar contains an entry for this variant (Variation ID: 591573). This variant has not been reported in the literature in individuals affected with SLX4-related conditions. This variant is not present in population databases (gnomAD no frequency). This sequence change creates a premature translational stop signal (p.Ser1608*) in the SLX4 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in SLX4 are known to be pathogenic (PMID: 21240277). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV003411662 | SCV004111213 | likely pathogenic | SLX4-related disorder | 2022-12-13 | criteria provided, single submitter | clinical testing | The SLX4 c.4823C>G variant is predicted to result in premature protein termination (p.Ser1608*). To our knowledge, this variant has not been reported in the literature or in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Nonsense variants in SLX4 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |
Gharavi Laboratory, |
RCV000722754 | SCV000853885 | uncertain significance | not provided | 2018-09-16 | no assertion criteria provided | research |