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Multiomic Single-Cell Sequencing Identifies BCR::ABL1 as an Acquired Resistance Mechanism in FLT3+ AML
Vanessa E Kennedy1, Cheryl A C Peretz2, Andrew Koh3
1Department of Medicine, Stanford University, Stanford, California, USA.
European Journal of Haematology
|April 28, 2026
Summary
BCR::ABL1 acquisition is a new resistance mechanism in FLT3-mutated acute myeloid leukemia (AML). This study used single-cell sequencing to show BCR::ABL1 emerged alongside FLT3-ITD, driving FLT3 inhibitor resistance in specific AML cells.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- Acute myeloid leukemia (AML) with FLT3 mutations presents a therapeutic challenge.
- Emerging resistance mechanisms, such as BCR::ABL1 acquisition, complicate treatment strategies.
- Understanding clonal evolution is crucial for overcoming treatment resistance in FLT3-mutated AML.
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