Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Fulgent Genetics, |
RCV002496419 | SCV002806017 | pathogenic | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2021-09-27 | criteria provided, single submitter | clinical testing | |
Labcorp Genetics |
RCV002496419 | SCV004569107 | pathogenic | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2022-12-01 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Lys3067Argfs*2) in the APOB gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in APOB are known to be pathogenic (PMID: 20032471). This variant is not present in population databases (gnomAD no frequency). This premature translational stop signal has been observed in individual(s) with hypobetalipoproteinemia (PMID: 2022744). This variant is also known as a single nucleotide deletion in exon 26 (cDNA nucleotide 9327). ClinVar contains an entry for this variant (Variation ID: 17892). For these reasons, this variant has been classified as Pathogenic. |
Gene |
RCV005003395 | SCV005628314 | pathogenic | not provided | 2024-07-16 | criteria provided, single submitter | clinical testing | Frameshift variant predicted to result in protein truncation or nonsense mediated decay in a gene for which loss of function is a known mechanism of disease; Not observed at significant frequency in large population cohorts (gnomAD); Also known as apo B67; This variant is associated with the following publications: (PMID: 34570182, 2022744) |
OMIM | RCV000019481 | SCV000039777 | pathogenic | Familial hypobetalipoproteinemia | 1991-05-01 | no assertion criteria provided | literature only |