Regulation of autophagy in hematological malignancies: role of reactive oxygen species

Abstract

Hematological malignancies are characterized by the accumulation of lymphoid and myeloid cell types due to selective proliferation and survival in blood, bone marrow and lymph nodes. Treatments of hematological malignancies are often effective but eventually relapse, and drug resistance occurs. A better understanding of the mechanism of action of both chemotherapeutic drugs and drug resistance is required. Autophagy has been shown to regulate both cell survival and cell death, leading to both cancer development and tumor suppression. In addition, many chemotherapeutic drugs induce autophagy, leading to either drug resistance or cell death. Autophagy is regulated by signaling pathways such as p53 and by the production of reactive oxygen species (ROS). This review focuses on the regulation of autophagy in human hematologic malignancy leading to either cell survival or death. In addition, the role that ROS play in regulating autophagy and its implication for hematological cancers is discussed.

Keywords::

• Autophagy
• survival
• cell death
• reactive oxygen species
• signal transduction

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