Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001852022 | SCV002229408 | pathogenic | Bardet-Biedl syndrome | 2023-12-25 | criteria provided, single submitter | clinical testing | This sequence change affects an acceptor splice site in intron 3 of the BBS2 gene. RNA analysis indicates that disruption of this splice site induces altered splicing and likely results in a shortened protein product. This variant is not present in population databases (gnomAD no frequency). Disruption of this splice site has been observed in individual(s) with Bardet-Biedl syndrome (PMID: 20618352, 22981120). It is commonly reported in individuals of Hutterite ancestry (PMID: 20618352, 22981120). ClinVar contains an entry for this variant (Variation ID: 30550). Studies have shown that disruption of this splice site results in skipping of exon 4 and exons 3-4, but is expected to preserve the integrity of the reading-frame (PMID: 20618352). For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004532399 | SCV004117545 | pathogenic | BBS2-related disorder | 2023-08-04 | criteria provided, single submitter | clinical testing | The BBS2 c.472-2A>G variant is predicted to disrupt the AG splice acceptor site and interfere with normal splicing. This variant was reported in multiple individuals with Bardet-Biedl syndrome and is well known founder mutation in Hutterite population (Innes et al. 2010. PubMed ID: 20618352; Chong et al. 2012. PubMed ID: 22981120). This variant is reported in 0.00088% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/16-56544835-T-C). Variants that disrupt the consensus splice acceptor site in BBS2 are expected to be pathogenic. This variant is interpreted as pathogenic. |
OMIM | RCV000023507 | SCV000044798 | pathogenic | Bardet-Biedl syndrome 2 | 2012-10-05 | no assertion criteria provided | literature only |