Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV004700884 | SCV005205697 | likely pathogenic | Hereditary thrombocytopenia and hematologic cancer predisposition syndrome | 2024-09-10 | reviewed by expert panel | curation | NM_001754.5(RUNX1):c.385_395del (p.Leu129AspfsTer5) is a frameshift variant that occurs which terminates 5 amino acids downstream and is predicted to undergo NMD (As per modified RUNX1 PVS1 decision tree ) (PVS1_Strong). This variant is completely absent from all population databases with at least 20x coverage for RUNX1 (PM2_supporting). This variant is a frameshift variant that is downstream of c.98 (PM5_Supporting). In summary, this variant meets the criteria to be classified as likely pathogenic. ACMG/AMP criteria applied, as specified by the Myeloid Malignancy Variant Curation Expert Panel for RUNX1: PVS1_strong, PM2_supporting, PM5_supporting. |
Labcorp Genetics |
RCV002996576 | SCV003313580 | pathogenic | Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1 | 2022-02-03 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Leu129Aspfs*5) in the RUNX1 gene. It is expected to result in an absent or disrupted protein product. Loss-of-function variants in RUNX1 are known to be pathogenic (PMID: 18723428, 24100448). For these reasons, this variant has been classified as Pathogenic. This variant has not been reported in the literature in individuals affected with RUNX1-related conditions. This variant is not present in population databases (gnomAD no frequency). |