Leukemia, Philadelphia chromosome-positive, resistant to imatinib: genes and variants

Leukemia, Philadelphia chromosome-positive, resistant to imatinib is linked to 1 analyzed protein (ABL1). 5 DNA variants are known to cause it; 0 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 Leukemia, Philadelphia chromosome-positive, resistant to imatinib

Where Leukemia, Philadelphia chromosome-positive, resistant to imatinib variants cluster

Known disease-causing variants in Leukemia, Philadelphia chromosome-positive, resistant to imatinib

VariantPositionProtein partClinical label
ABL1 E255K255Protein kinaseDisease-causing
ABL1 E255V255Protein kinaseDisease-causing
ABL1 E236K236Disease-causing
ABL1 E236V236Disease-causing
ABL1 Y253H253Protein kinaseDisease-causing

Same protein, different disease

Diseases related to Leukemia, Philadelphia chromosome-positive, resistant to imatinib

Frequently asked questions

Which genes are linked to Leukemia, Philadelphia chromosome-positive, resistant to imatinib?

In CATVariant, Leukemia, Philadelphia chromosome-positive, resistant to imatinib is linked to 1 analyzed protein: ABL1 (Tyrosine-protein kinase ABL1).

How many genetic variants are linked to Leukemia, Philadelphia chromosome-positive, resistant to imatinib?

5 variants: 5 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 0 are of uncertain significance or have conflicting reports.

Which uncertain variants in Leukemia, Philadelphia chromosome-positive, resistant to imatinib 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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