Imatinib Resistance in Chronic Myeloid Leukemia Is Associated with Distinct Metabolic, Oxidative, and Autophagic Adaptations in K562-Derived Cell Sublines

Background/Objectives: Chronic myeloid leukemia (CML) is a hematopoietic stem cell malignancy initiated by the BCR::ABL1 oncoprotein. Although tyrosine kinase inhibitors (TKIs) have revolutionized CML therapy, resistance remains a major clinical challenge. Emerging evidence suggests that metabolic reprogramming contributes to TKI resistance, yet its relationship with oxidative stress and autophagy remains poorly characterized.