Total submissions: 6
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000671341 | SCV000796305 | uncertain significance | Bardet-Biedl syndrome 12 | 2017-12-11 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001046755 | SCV001210669 | likely pathogenic | Bardet-Biedl syndrome | 2023-12-06 | criteria provided, single submitter | clinical testing | This sequence change replaces proline, which is neutral and non-polar, with leucine, which is neutral and non-polar, at codon 159 of the BBS12 protein (p.Pro159Leu). This variant is present in population databases (no rsID available, gnomAD 0.002%). This missense change has been observed in individual(s) with BBS12-related conditions (PMID: 22410627, 25982971). ClinVar contains an entry for this variant (Variation ID: 555505). Advanced modeling of protein sequence and biophysical properties (such as structural, functional, and spatial information, amino acid conservation, physicochemical variation, residue mobility, and thermodynamic stability) performed at Invitae indicates that this missense variant is expected to disrupt BBS12 protein function with a positive predictive value of 80%. Experimental studies are conflicting or provide insufficient evidence to determine the effect of this variant on BBS12 function (PMID: 20080638, 20498079). In summary, the currently available evidence indicates that the variant is pathogenic, but additional data are needed to prove that conclusively. Therefore, this variant has been classified as Likely Pathogenic. |
Blueprint Genetics | RCV001074269 | SCV001239842 | likely pathogenic | Retinal dystrophy | 2019-05-14 | criteria provided, single submitter | clinical testing | |
Prevention |
RCV003420188 | SCV004109031 | uncertain significance | BBS12-related disorder | 2023-03-09 | criteria provided, single submitter | clinical testing | The BBS12 c.476C>T variant is predicted to result in the amino acid substitution p.Pro159Leu. This variant was reported in at least two individuals with Bardet-Biedl syndrome (Stoetzel et al. 2007. PubMed ID: 17160889; Scheidecker et al. 2015. PubMed ID: 25982971; Daniels et al. 2012. PubMed ID: 22410627; Chen et al. 2011. PubMed ID: 21642631). This variant is reported in 0.0023% of alleles in individuals of European (Non-Finnish) descent in gnomAD (http://gnomad.broadinstitute.org/variant/4-123663523-C-T). Functional studies are conflicting, one study concludes this variant as benign (Zaghloul NA et al 2010. PubMed ID: 20498079 Table S5), another study shows reduced protein interaction with BBS6, while interaction with BBS7 in unaffected (Seo et al. 2010. PubMed ID: 20080638). Although we suspect that this variant may be pathogenic, at this time, the clinical significance of this variant is uncertain due to the absence of conclusive functional and genetic evidence. |
Baylor Genetics | RCV000671341 | SCV004211695 | likely pathogenic | Bardet-Biedl syndrome 12 | 2024-02-20 | criteria provided, single submitter | clinical testing | |
Natera, |
RCV000671341 | SCV002082483 | uncertain significance | Bardet-Biedl syndrome 12 | 2020-10-14 | no assertion criteria provided | clinical testing |