Total submissions: 12
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Counsyl | RCV000667444 | SCV000791889 | pathogenic | Bardet-Biedl syndrome 2 | 2017-05-30 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV000667444 | SCV000918640 | pathogenic | Bardet-Biedl syndrome 2 | 2017-09-08 | criteria provided, single submitter | clinical testing | Variant summary: The BBS2 c.814C>T (p.Arg272X) variant results in a premature termination codon, predicted to cause a truncated or absent BBS2 protein due to nonsense mediated decay, which are commonly known mechanisms for disease. A truncation downstream of this position, c.823C>T (p.Arg275X) has been classified as pathogenic by our laboratory. This variant was found in 3/246118 control chromosomes at a frequency of 0.0000122, which does not exceed the estimated maximal expected allele frequency of a pathogenic BBS2 variant (0.0008452). Multiple publications have cited the variant in homozygous affected individuals. The variant of interest has not, to our knowledge, been cited and classified by clinical diagnostic laboratories. Taken together, this variant is classified as pathogenic. |
Labcorp Genetics |
RCV000808886 | SCV000949015 | pathogenic | Bardet-Biedl syndrome | 2023-06-26 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg272*) in the BBS2 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in BBS2 are known to be pathogenic (PMID: 11285252, 20177705, 24608809, 26518167). This variant is present in population databases (rs764164384, gnomAD 0.01%). This premature translational stop signal has been observed in individual(s) with Bardet-Biedl syndrome (PMID: 11285252, 28559085). ClinVar contains an entry for this variant (Variation ID: 552219). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV001528280 | SCV002558151 | pathogenic | not provided | 2022-02-03 | criteria provided, single submitter | clinical testing | Nonsense variant predicted to result in protein truncation or nonsense-mediated decay in a gene for which loss-of-function is a known mechanism of disease; This variant is associated with the following publications: (PMID: 25525159, 28559085, 25780760, 31196119, 11285252) |
Fulgent Genetics, |
RCV002499159 | SCV002810320 | pathogenic | Bardet-Biedl syndrome 2; Retinitis pigmentosa 74 | 2024-06-15 | criteria provided, single submitter | clinical testing | |
SN ONGC Dept of Genetics and Molecular biology Vision Research Foundation | RCV000808886 | SCV003915882 | pathogenic | Bardet-Biedl syndrome | criteria provided, single submitter | research | ||
Baylor Genetics | RCV000667444 | SCV004214012 | pathogenic | Bardet-Biedl syndrome 2 | 2023-09-07 | criteria provided, single submitter | clinical testing | |
Dept Of Ophthalmology, |
RCV003889949 | SCV004705070 | pathogenic | Retinal dystrophy | 2023-10-01 | criteria provided, single submitter | research | |
Natera, |
RCV000667444 | SCV001457441 | pathogenic | Bardet-Biedl syndrome 2 | 2020-09-16 | no assertion criteria provided | clinical testing | |
Diagnostic Laboratory, |
RCV001528280 | SCV001739755 | pathogenic | not provided | no assertion criteria provided | clinical testing | ||
Joint Genome Diagnostic Labs from Nijmegen and Maastricht, |
RCV001528280 | SCV001958376 | pathogenic | not provided | no assertion criteria provided | clinical testing | ||
Prevention |
RCV004732990 | SCV005356812 | pathogenic | BBS2-related disorder | 2024-09-20 | no assertion criteria provided | clinical testing | The BBS2 c.814C>T variant is predicted to result in premature protein termination (p.Arg272*). This variant was found in the homozygous state in multiple individuals with Bardet-Biedl syndrome (see family 4 from Nishimura et al. 2001. PubMed ID: 11285252; Hjortshøj et al. 2010. PubMed ID: 20120035; Redin et al. 2012. PubMed ID: 22773737). This variant is reported in 0.0099% of alleles in individuals of Ashkenazi Jewish descent in gnomAD. Nonsense variants in BBS2 are expected to be pathogenic. This variant is interpreted as pathogenic. |