A Novel BCR::ABL1 I502 T Mutation Associated With Acquired Asciminib Resistance in Chronic-Phase Chronic Myeloid Leukemia (SOHO 2026) - Sep 1, 2026 - Abstract #CML-1215; Location: LEVEL 3, HALL B3; "Case: A 41-year-old woman with CP-CML was initially treated with imatinib for 5 years before transitioning to nilotinib for molecular relapse...Critically, I502 T retained sensitivity to dasatinib (IC50 0.3 nM) and ponatinib (IC50 0.7 nM)... I502 T is a novel myristoyl pocket mutation that confers high-level asciminib resistance while retaining sensitivity to ATP-competitive TKIs, further expanding the landscape of resistance at this critical drug-binding interface. ATP: adenosine triphosphate, BCR::ABL1: breakpoint cluster region–Abelson murine leukemia viral oncogene homolog 1, ERK: extracellular signal-regulated kinase, IC50: half-maximal inhibitory concentration, S6: ribosomal protein S6, STAT5: signal transducer and activator of transcription 5, VAF: variant allele frequency, WT: wild-type."
Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology • ABL1 • BCR • RPS6 • STAT5
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Murugan Selvam PhD 1; Rahul Kumar Thakur MD 1; Evan Lee BS 2; Laurie Horsch MD 2; Leslie Martinez-Gutierrez BS 1; Eunice S Wang MD 1; Pamela J Sung MD PhD 1
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