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Updated: Mar 18, 2026

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors
Published on: October 17, 2025
Recent advances and novel agents for FLT3 mutated acute myeloid leukemia
Rahul Pawar1, Omar Preet Singh Bali1, Bharat Kumar Malhotra1
11 Department of Medicine, New York Medical College, Valhalla, NY 10595, USA ; 2 King Edward Memorial Hospital, Acharya Donde Marg, Parel, Mumbai 400 012, India ; 3 Department of Medicine, KU School of Medicine-Wichita, Wichita, KS 67214, USA ; 4 Department of Medicine, University of Vermont, Burlington, VT 05405, USA.
Abstract:
Acute myeloid leukemia (AML) is a devastating hematologic malignancy that affects both older adults as well as children. Treatments available for AML largely depend on cytotoxic agents and often the only curative option is an allogeneic bone marrow transplant, an option limited to young persons and associated with high morbidity and mortality. There is an urgent need for the identification of new myeloid targets and an understanding of the key genetic mutations involved in disease progression and prognosis. One such mutation is the internal tandem duplication (ITD) in the FMS-like tyrosine kinase receptor-3 (FLT3) gene which confers an inferior outcome that is attributed to a higher relapse rate. In this review, we evaluate the FLT3-ITD mutation and discuss the recent data regarding emerging approaches using FLT3 inhibitors for the treatment of AML.
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