N 6 -methyladenosine (m 6 A) RNA modification in chronic myeloid leukemia: unveiling a novel therapeutic target.

N 6 -methyladenosine (m 6 A), 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, m 6 A has garnered significant attention for a deeper understanding of the initiation, progression, and drug resistance of various cancers, including hematological malignancies. Dysregulation of m 6 A has been implicated in both cancer promotion and suppression. m 6 A methylation is a complex regulatory process involving methyltransferases (writers), demethylases (erasers), and proteins that recognize specific m 6 A modifications (readers). This intricate interplay presents challenges for precisely modulating m 6 A levels, either globally or at specific sites. This review specifically focuses on the role of m 6 A 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 m 6 A regulators show promise in preclinical models, suggesting a potential therapeutic avenue for CML. Integrating our understanding of m 6 A biology with current treatment strategies may lead to more effective therapies, especially for patients with advanced-stage or resistant CML.