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Transcriptomic differences in cabozantinib-resisant AML cells.

GSE234724 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2026/02/25 Platform GPL18573
Summary
Cabozantinib is a type II tyrosine kinase inhibitor (TKI), which is approved by FDA for treating several solid tumors including advanced/progressive metastatic medullar thyroid cancer, advanced renal cell carcinoma, and advanced and progressive hepatocellular carcinoma. Moreover, we and others revealed its cytotoxicity on FLT3-ITD, KIT-driven t(8;21) AML cells, and its efficacy on promoting erythroid differentiation of leukemic cell line K562. A clinical trial report also suggested that cabozantinib is well tolerated in FLT3-ITD AML patients. While those findings highlighted the feasibility of cabozantinib targeting specific AML subtypes, it is unclear whether cabozantinib treatment arises resistance in cancer cells. To identify the mechanism and transcriptomic change of cabozantinib resistance, we established drug-resistant cell lines by culturing Molm13 and MV4-11 leukemic cell lines in increasing drug concentrations.
Published in
Modulating metabolic signatures to mitigate cabozantinib resistance in FLT3-ITD acute myeloid leukemia cell models
Fu YH, Ng KM, Tseng CY et al. · Cell death discovery 2026 · PMID 41702887 · doi:10.1038/s41420-026-02957-8
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Also filed as BioProject PRJNA982820 and SRA study SRP442913. Searching any of these in the dataset finder brings you back here.

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