Inflammation, ROS, and Mutagenesis

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Inflammation, ROS, and Mutagenesis Asmaa El-Kenawi, Brian Ruffell  Cancer Cell  Volume 32, Issue 6, Pages 727-729 (December 2017) DOI: 10.1016/j.ccell.2017.11.015 Copyright © 2017 Elsevier Inc. Terms and Conditions

Figure 1 Myeloid-Cell-Derived ROS Promotes Inflammation and Mutagenesis (A) During acute inflammation, the production of ROS (such as H2O2) by myeloid cells promotes apoptosis of damaged cells, wound repair and a return to tissue homeostasis. (B) As a consequence of Gpx4-deficiency in macrophages and/or neutrophils, increased production of extracellular ROS leads to oxidative stress within epithelial cells and the accumulation of oncogenic mutations. ROS production also creates a positive feedback loop via autocrine TNF-α-mediated expression of inflammatory cytokines/chemokines (data not shown), and the combination of these two pathways drives neoplastic progression. Cancer Cell 2017 32, 727-729DOI: (10.1016/j.ccell.2017.11.015) Copyright © 2017 Elsevier Inc. Terms and Conditions