Identification of a Chemoresistant “Oxidative State-Low” Leukemic Subpopulation in CD34+ Human Acute Myeloid Leukemia

Abstract

Reactive oxygen species (ROS) are oxygen-containing side products of normal aerobic metabolism. Although it was initially believed that ROS constitute only damaging by-products, recent evidence suggest that ROS actively participate in signal transduction pathways and regulate cell survival and proliferation in a dose-depended manner [1,2]. Endogenous intracellular redox state is tightly controlled by free radical scavenging systems and the appropriate ROS levels differ among cell types and differentiation status [3]. Hematopoietic stem cells (HSCs) in mice reside mainly in the ROSlow subset of hematopoietic progenitors [4], whereas forced increase of ROS in human Lin-CD34+CD38cord blood cells leads to loss of stem cell activity [5-7]. Similarly, though increased ROS levels in tumor cells have been implicated in cancer initiation and progression.

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Cite this paper

@inproceedings{Kotsianidis2014IdentificationOA, title={Identification of a Chemoresistant “Oxidative State-Low” Leukemic Subpopulation in CD34+ Human Acute Myeloid Leukemia}, author={Ioannis Kotsianidis and Dimitra Kokkinou and Elena Konstantina Siapati and Paraskevi Miltiades and Eleftheria E. Lamprianidou and George Vassilopoulos and Alexandros Spyridonidis}, year={2014} }