Total submissions: 5
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
LDLR- |
RCV000211573 | SCV000295574 | pathogenic | Hypercholesterolemia, familial, 1 | 2016-03-25 | criteria provided, single submitter | literature only | |
Laboratory of molecular diagnosis of dyslipidemias, |
RCV000211573 | SCV001653644 | pathogenic | Hypercholesterolemia, familial, 1 | 2021-05-24 | criteria provided, single submitter | clinical testing | |
Women's Health and Genetics/Laboratory Corporation of America, |
RCV003488470 | SCV004240815 | pathogenic | Familial hypercholesterolemia | 2023-12-11 | criteria provided, single submitter | clinical testing | Variant summary: LDLR c.1685G>A (p.Trp562X) results in a premature termination codon and is expected to cause absence of the protein due to nonsense mediated decay, a commonly known mechanism for disease. The variant was absent in 251416 control chromosomes (gnomAD). c.1685G>A has been reported in the literature in individuals affected with Familial Hypercholesterolemia and segregated with the disease phenotype (e.g. Marduel_2010). These data indicate that the variant is very likely associated with disease. The following publication has been ascertained in the context of this evaluation (PMID: 20809525). Two submitters have cited clinical-significance assessments for this variant to ClinVar after 2014. Both submitters classified the variant as pathogenic. Based on the evidence outlined above, the variant was classified as pathogenic. |
Cardiovascular Genetics Laboratory, |
RCV000211573 | SCV000268627 | pathogenic | Hypercholesterolemia, familial, 1 | 2011-11-07 | no assertion criteria provided | clinical testing | |
Laboratorium voor Moleculaire Diagnostiek Experimentele Vasculaire Geneeskunde, |
RCV000211573 | SCV000606482 | pathogenic | Hypercholesterolemia, familial, 1 | no assertion criteria provided | research |