Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Labcorp Genetics |
RCV001838454 | SCV001394937 | benign | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2023-10-04 | criteria provided, single submitter | clinical testing | |
Institute of Human Genetics, |
RCV001262466 | SCV001440358 | uncertain significance | Hypercholesterolemia, autosomal dominant, type B | 2019-01-01 | criteria provided, single submitter | clinical testing | |
Ambry Genetics | RCV002447120 | SCV002734362 | uncertain significance | Cardiovascular phenotype | 2022-03-11 | criteria provided, single submitter | clinical testing | The p.P771L variant (also known as c.2312C>T), located in coding exon 16 of the APOB gene, results from a C to T substitution at nucleotide position 2312. The proline at codon 771 is replaced by leucine, an amino acid with similar properties. This amino acid position is highly conserved in available vertebrate species. In addition, the in silico prediction for this alteration is inconclusive. Since supporting evidence is limited at this time, the clinical significance of this alteration remains unclear. |
Fulgent Genetics, |
RCV001838454 | SCV002787863 | uncertain significance | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2021-08-03 | criteria provided, single submitter | clinical testing | |
Gene |
RCV003327498 | SCV004034756 | uncertain significance | not provided | 2023-09-06 | criteria provided, single submitter | clinical testing | Has not been previously published as pathogenic or benign to our knowledge; In silico analysis supports that this missense variant has a deleterious effect on protein structure/function |