Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
LDLR- |
RCV000237666 | SCV000295905 | pathogenic | Hypercholesterolemia, familial, 1 | 2016-03-25 | criteria provided, single submitter | literature only | |
Institute of Human Genetics, |
RCV000237666 | SCV001950087 | pathogenic | Hypercholesterolemia, familial, 1 | 2023-02-14 | criteria provided, single submitter | clinical testing | This variant was identified as compound heterozygous with NM_000527.5:c.397G>T._x000D_ Criteria applied: PVS1, PS4_MOD, PM2_SUP |
Ambry Genetics | RCV002429176 | SCV002731349 | pathogenic | Cardiovascular phenotype | 2019-07-08 | criteria provided, single submitter | clinical testing | The c.2167delG pathogenic mutation, located in coding exon 15 of the LDLR gene, results from a deletion of one nucleotide at nucleotide position 2167, causing a translational frameshift with a predicted alternate stop codon (p.E723Rfs*7). This alteration has been detected in an individual with hypercholesterolemia (Bochmann H et al. Hum. Mutat., 2001;17:76-7). This alteration is expected to result in loss of function by premature protein truncation or nonsense-mediated mRNA decay. As such, this alteration is interpreted as a disease-causing mutation. |