Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000668445 | SCV000793050 | likely pathogenic | Bardet-Biedl syndrome 2 | 2017-08-01 | criteria provided, single submitter | clinical testing | |
Revvity Omics, |
RCV001784253 | SCV002024473 | pathogenic | not provided | 2019-10-29 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV000668445 | SCV004214065 | pathogenic | Bardet-Biedl syndrome 2 | 2022-01-03 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV003523007 | SCV004297728 | pathogenic | Bardet-Biedl syndrome | 2023-12-06 | criteria provided, single submitter | clinical testing | This sequence change affects a donor splice site in intron 6 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 present in population databases (no rsID available, gnomAD 0.0009%). Disruption of this splice site has been observed in individual(s) with clinical features of Bardet-Biedl syndrome (PMID: 28717663). ClinVar contains an entry for this variant (Variation ID: 553071). Studies have shown that disruption of this splice site results in skipping of exon 6, but is expected to preserve the integrity of the reading-frame (PMID: 28717663). This variant disrupts a region of the BBS2 protein in which other variant(s) (p.Leu221Pro) have been observed in individuals with BBS2-related conditions (PMID: 20177705). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. For these reasons, this variant has been classified as Pathogenic. |
Fulgent Genetics, |
RCV005019126 | SCV005644059 | pathogenic | Bardet-Biedl syndrome 2; Retinitis pigmentosa 74 | 2024-03-08 | criteria provided, single submitter | clinical testing |