Total submissions: 7
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
LDLR- |
RCV000211601 | SCV000294849 | pathogenic | Hypercholesterolemia, familial, 1 | 2016-03-25 | criteria provided, single submitter | literature only | |
Robarts Research Institute, |
RCV000211601 | SCV000484804 | likely pathogenic | Hypercholesterolemia, familial, 1 | criteria provided, single submitter | clinical testing | ||
U4M - |
RCV000211601 | SCV000583713 | pathogenic | Hypercholesterolemia, familial, 1 | 2017-03-30 | criteria provided, single submitter | clinical testing | |
Molecular Diagnostic Laboratory for Inherited Cardiovascular Disease, |
RCV001256904 | SCV001433409 | pathogenic | not provided | 2019-02-26 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV001389664 | SCV001591109 | pathogenic | Familial hypercholesterolemia | 2023-07-14 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Asp217*) in the LDLR gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in LDLR are known to be pathogenic (PMID: 20809525, 28645073). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hypercholesterolemia (PMID: 19446849). ClinVar contains an entry for this variant (Variation ID: 226328). For these reasons, this variant has been classified as Pathogenic. |
Laboratory of molecular diagnosis of dyslipidemias, |
RCV000211601 | SCV001653605 | pathogenic | Hypercholesterolemia, familial, 1 | 2021-05-24 | criteria provided, single submitter | clinical testing | |
Cardiovascular Genetics Laboratory, |
RCV000211601 | SCV000268573 | pathogenic | Hypercholesterolemia, familial, 1 | 2014-08-14 | no assertion criteria provided | clinical testing |