Total submissions: 3
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Brunham Lab, |
RCV001255949 | SCV001432654 | pathogenic | Hypercholesterolemia, familial, 1 | 2019-03-13 | criteria provided, single submitter | research | |
Labcorp Genetics |
RCV001879948 | SCV002234159 | pathogenic | Familial hypercholesterolemia | 2022-07-25 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Val498Leufs*37) 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). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 977993). This premature translational stop signal has been observed in individual(s) with familial hypercholesterolemia (PMID: 31345425). |
Prevention |
RCV003405465 | SCV004106774 | pathogenic | LDLR-related disorder | 2023-03-24 | criteria provided, single submitter | clinical testing | The LDLR c.1492_1493delGT variant is predicted to result in a frameshift and premature protein termination (p.Val498Leufs*37). This variant has been reported in at least one individual with Familial Hypercholesterolemia (Trinder et al. 2019. PubMed ID: 31345425. Online Table 3). This variant has not been reported in a large population database (http://gnomad.broadinstitute.org), indicating this variant is rare. Frameshift variants in LDLR are expected to be pathogenic. This variant is interpreted as pathogenic. |