Total submissions: 4
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Ce |
RCV001093352 | SCV001250290 | pathogenic | not provided | 2019-11-01 | criteria provided, single submitter | clinical testing | |
DASA | RCV001181782 | SCV002061185 | likely pathogenic | Familial hypercholesterolemia | 2022-01-05 | criteria provided, single submitter | clinical testing | The variant creates a premature translational stop signal c.6253C>T;p.(Arg2085*) in APOB gene. It is expected to result in an absent or disrupted protein product - PVS1.This variant is not present in population databases (rs121918386, gnomAD; ABraOM no frequency - http://abraom.ib.usp.br/) - PM2. In summary, the currently available evidence indicates that the variant is likely pathogenic. |
Labcorp Genetics |
RCV001851947 | SCV002230906 | pathogenic | Hypercholesterolemia, autosomal dominant, type B; Familial hypobetalipoproteinemia 1 | 2022-03-15 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Arg2085*) 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 present in population databases (rs121918386, gnomAD 0.004%). For these reasons, this variant has been classified as Pathogenic. ClinVar contains an entry for this variant (Variation ID: 17887). This variant is also known as C to T at nucleotide 6381. This premature translational stop signal has been observed in individual(s) with familial hypobetalipoproteinemia (PMID: 2725600). |
OMIM | RCV000019476 | SCV000039769 | pathogenic | Familial hypobetalipoproteinemia | 1989-06-15 | no assertion criteria provided | literature only |