Total submissions: 2
Submitter | RCV | SCV | Clinical significance | Condition | Last evaluated | Review status | Method | Comment |
---|---|---|---|---|---|---|---|---|
Clin |
RCV004701771 | SCV005205627 | likely pathogenic | Hereditary thrombocytopenia and hematologic cancer predisposition syndrome | 2024-08-28 | reviewed by expert panel | curation | NM_001754.5(RUNX1):c.551_552insTACCACAGAGCCATCTGTG (p.Gln185ThrfsTer34) is a frameshift variant which terminates 34 amino acids downstream and is predicted to undergo nonsense-mediated decay (PVS1_Strong). This variant is completely absent from all population databases with at least 20x coverage for RUNX1 (PM2_supporting). It 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 |
RCV003630269 | SCV004406079 | pathogenic | Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1 | 2022-12-03 | criteria provided, single submitter | clinical testing | This sequence change creates a premature translational stop signal (p.Gln185Thrfs*34) 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). |