ArticleScientific reports2026
Busulfan resistance in AML is associated with changes in mitochondrial copy number and lipid metabolism.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Busulfan (BU) is DNA-damaging and also a reactive oxygen species (ROS) generating agent. Both mitochondrial DNA copy number (mtDNA-CN) and ROS levels have been associated with the sensitivity of solid tumor cells to ROS-generating cisplatin. However, the changes of mtDNA-CN during the development of resistance to other ROS-generating agents or chemotherapeutics remain unclear. In this study, we investigated how the resistance of acute myeloid leukemia (AML) cell lines to the BU or the DNA synthesis inhibitor cytarabine (Cyt) is associated with alterations in mtDNA-CN and global gene expression. To follow BU resistance acquisition, MOLM13 myeloid leukemia cells, which are sensitive to BU, were subjected to five consecutive BU treatment rounds, generating BU-resistant cells (5TBU). Both parental control cells and the 5TBU cells underwent five consecutive Cyt treatments to generate cells resistant to both Bu and Cyt. We assessed mtDNA-CN using RT-qPCR targeting the mitochondrial gene MTND1 and investigated global gene expression profiles using bulk RNA-sequencing before and after resistance acquisition. We estimated the BU 50% inhibitory concentration (BU-IC
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