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Acute lymphoblastic leukemia (ALL) is a heterogeneous malignancy driven by diverse genetic alterations. The BCR::ABL1-positive subtype and ABL-class subtype, each accounting for ∼3% of newly diagnosed pediatric ALL cases, involve fusions with ABL family tyrosine kinase genes.1 In this study, the ABL-class subtype was defined as fusions involving tyrosine kinases ABL1, ABL2, PDGFRB, or CSF1R fused to various partner genes, excluding the sentinel BCR::ABL1 fusion.
BCR::ABL1–positive B-cell precursor acute lymphoblastic leukemia (BCP-ALL), also known as Philadelphia chromosome–positive BCP-ALL, is characterized by the t(9;22)(q34;q11) translocation.
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