Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Brunham Lab, |
RCV001255937 | SCV001432582 | pathogenic | Hypercholesterolemia, familial, 1 | 2019-01-25 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV002534034 | SCV003249625 | uncertain significance | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2022-08-10 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Tyr4232*) in the APOB gene. While this is not anticipated to result in nonsense mediated decay, it is expected to disrupt the last 332 amino acid(s) of the APOB protein. This variant is present in population databases (no rsID available, gnomAD 0.0009%). This premature translational stop signal has been observed in individual(s) with familial hypercholesterolemia (PMID: 31345425). ClinVar contains an entry for this variant (Variation ID: 628375). This variant disrupts a region of the APOB protein in which other variant(s) (p.Tyr4380*) have been observed in individuals with APOB-related conditions (Invitae). This suggests that this is a clinically significant region of the protein, and that variants that disrupt it are likely to be disease-causing. In summary, the available evidence is currently insufficient to determine the role of this variant in disease. Therefore, it has been classified as a Variant of Uncertain Significance. |
Baylor Genetics | RCV003147545 | SCV003835384 | likely pathogenic | Hypercholesterolemia, autosomal dominant, type B | 2022-11-04 | criteria provided, single submitter | clinical testing | |
Baylor Genetics | RCV003147546 | SCV003836005 | likely pathogenic | Familial hypobetalipoproteinemia 1 | 2022-11-04 | criteria provided, single submitter | clinical testing | |
Lildballe Lab, |
RCV004773127 | SCV005200539 | likely pathogenic | Hypercholesterolemia | 2024-03-01 | criteria provided, single submitter | research | PS4(sup), PM2(sup), pVS1(m) |