Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Eurofins Ntd Llc |
RCV000593549 | SCV000708488 | pathogenic | not provided | 2017-05-08 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV000593549 | SCV000942214 | pathogenic | not provided | 2024-11-21 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg220Valfs*37) in the ABCG8 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in ABCG8 are known to be pathogenic (PMID: 11452359, 15375183, 16029460). This variant is present in population databases (no rsID available, gnomAD 0.06%). This premature translational stop signal has been observed in individual(s) with ABCG8 (internal data). It has also been observed to segregate with disease in related individuals. ClinVar contains an entry for this variant (Variation ID: 501952). Algorithms developed to predict the effect of sequence changes on RNA splicing suggest that this variant may disrupt the consensus splice site. For these reasons, this variant has been classified as Pathogenic. |
Prevention |
RCV004742533 | SCV005364944 | likely pathogenic | ABCG8-related disorder | 2024-09-06 | no assertion criteria provided | clinical testing | The ABCG8 c.647_657dup11 variant is predicted to result in a frameshift and premature protein termination (p.Arg220Valfs*37). To our knowledge, this variant has not been reported in the literature. This variant is reported in 0.064% of alleles in individuals of Latino descent in gnomAD. Frameshift variants in ABCG8 are expected to be pathogenic. This variant is interpreted as likely pathogenic. |