N-methyladenosine (mA) RNA modification in chronic myeloid leukemia: unveiling a novel therapeutic target.

N-methyladenosine (mA), the most prevalent internal mRNA modification, plays a critical role in physiological processes by regulating gene expression through modulation of mRNA metabolism at multiple stages. In recent years, mA has garnered significant attention for a deeper understanding of the initiation, progression, and drug resistance of various cancers, including hematological malignancies. Dysregulation of mA has been implicated in both cancer promotion and suppression. mA methylation is a complex regulatory process involving methyltransferases (writers), demethylases (erasers), and proteins that recognize specific mA modifications (readers). This intricate interplay presents challenges for precisely modulating mA levels, either globally or at specific sites. This review specifically focuses on the role of mA in chronic myeloid leukemia (CML), a blood cancer characterized by the BCR-ABL1 fusion. We emphasize its impact on leukemia cell survival and drug resistance mechanisms. Notably, inhibitors targeting mA regulators show promise in preclinical models, suggesting a potential therapeutic avenue for CML. Integrating our understanding of mA biology with current treatment strategies may lead to more effective therapies, especially for patients with advanced-stage or resistant CML.