Reactive oxygen species in haematopoiesis: leukaemic cells take a walk on the wild side

J Exp Clin Cancer Res. 2018 Jun 26;37(1):125. doi: 10.1186/s13046-018-0797-0.


Oxidative stress is related to ageing and degenerative diseases, including cancer. However, a moderate amount of reactive oxygen species (ROS) is required for the regulation of cellular signalling and gene expression. A low level of ROS is important for maintaining quiescence and the differentiation potential of haematopoietic stem cells (HSCs), whereas the level of ROS increases during haematopoietic differentiation; thus, suggesting the importance of redox signalling in haematopoiesis. Here, we will analyse the importance of ROS for haematopoiesis and include evidence showing that cells from leukaemia patients live under oxidative stress. The potential sources of ROS will be described. Finally, the level of oxidative stress in leukaemic cells can also be harnessed for therapeutic purposes. In this regard, the reliance of front-line anti-leukaemia chemotherapeutics on increased levels of ROS for their mechanism of action, as well as the active search for novel compounds that modulate the redox state of leukaemic cells, will be analysed.

Keywords: Haematopoietic stem cells (HSCs); Leukaemia; Mitochondria; NADPH oxidase (Nox); Oxidative stress; Reactive oxygen species (ROS); Redox signalling.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Biomarkers
  • Cell Differentiation / drug effects
  • Hematopoiesis* / drug effects
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / metabolism*
  • Humans
  • Leukemia / drug therapy
  • Leukemia / genetics
  • Leukemia / metabolism
  • Leukemia / pathology
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Molecular Targeted Therapy
  • NADPH Oxidases / genetics
  • NADPH Oxidases / metabolism
  • Oxidation-Reduction
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / drug effects


  • Antineoplastic Agents
  • Biomarkers
  • Reactive Oxygen Species
  • NADPH Oxidases