Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV002000219 | SCV002234023 | pathogenic | Bardet-Biedl syndrome | 2023-10-18 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg504*) in the BBS7 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BBS7 are known to be pathogenic (PMID: 12567324, 19402160, 21209035, 31196119). This variant is not present in population databases (gnomAD no frequency). This variant has not been reported in the literature in individuals affected with BBS7-related conditions. ClinVar contains an entry for this variant (Variation ID: 1453288). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may create or strengthen a splice site. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004744177 | SCV005354743 | likely pathogenic | BBS7-related disorder | 2024-09-03 | no assertion criteria provided | clinical testing | The BBS7 c.1510A>T variant is predicted to result in premature protein termination (p.Arg504*). To our knowledge, this variant has not been reported in the literature or a large population database, indicating it is rare. Nonsense variants in BBS7 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |