Novel roles of reactive oxygen species in the pathogenesis of acute myeloid leukemia.

It has become apparent that regulation of ROS is important in cell signaling and homeostasis. Accumulation of ROS triggers oxidative stress in various cell types and contributes to the development, progression, and persistence of cancer. Recent research has demonstrated that redox dysregulation caused by ROS promotes proliferation, differentiation, genomic, and epigenetic alterations; immune evasion; and survival in leukemic cells. ROS act as signaling molecules to regulate redox-sensitive transcriptional factors, enzymes, oncogenes, and other downstream effectors. Thus, a thorough understanding the role of ROS as key mediators in leukemogenesis is likely to provide opportunities for improved pharmacological intervention. In this review, we summarize the recent findings that support a role for ROS in the pathogenesis of AML and outline innovative approaches in the implementation of redox therapies for myeloid malignancies.