Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1: genes and variants

Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1 is linked to 1 analyzed protein (RUNX1). 3 DNA variants are known to cause it; 37 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1

Known disease-causing variants in Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1

VariantPositionProtein partClinical label
RUNX1 H78P78RuntDisease-causing (★★★)
RUNX1 R142I142RuntDisease-causing (★★★)
RUNX1 S67R67RuntDisease-causing (★★★)

Same protein, different disease

Diseases related to Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1

Frequently asked questions

Which genes are linked to Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1?

In CATVariant, Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1 is linked to 1 analyzed protein: RUNX1 (Runt-related transcription factor 1).

How many genetic variants are linked to Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1?

66 variants: 3 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 37 are of uncertain significance or have conflicting reports.

Which uncertain variants in Hereditary thrombocytopenia and hematological cancer predisposition syndrome associated with RUNX1 look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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