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Review
. 2018 Aug 1;10(8):a028662.
doi: 10.1101/cshperspect.a028662.

Cancer Inflammation and Cytokines

Maria Rosaria Galdiero  1 , Gianni Marone  1   2 , Alberto Mantovani  3   4
Affiliations
Review

Cancer Inflammation and Cytokines

Maria Rosaria Galdiero et al. Cold Spring Harb Perspect Biol. .

Abstract

Chronic inflammation is a well-recognized tumor-enabling capability, which allows nascent tumors to escape immunosurveillance. A number of soluble and cellular inflammatory mediators take part in the various phases of cancer initiation and progression, giving rise to a fatal conspiracy, which is difficult to efficiently overcome. Tumor-associated macrophages (TAMs) are pivotal players of the tumor microenvironment and, because of their characteristic plasticity, can acquire a number of distinct phenotypes and contribute in different ways to the various phases of cancerogenesis. Tumor-associated neutrophils (TANs) are also emerging as important components of the tumor microenvironment, given their unexpected heterogeneity and plasticity. TAMs and TANs are both integrated in cancer-related inflammation and an ever better understanding of their functions can be useful to tailor the use of anticancer therapeutic approaches and patient follow-up.

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Figures

Figure 1.
Figure 1.
Tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) as key regulators of the tumor-related inflammation. Neoplastic and stromal cells recruit macrophages and neutrophils, favoring their polarization toward a protumor phenotype. In turn, TAMs and TANs induce genetic instability (through the release of reactive oxygen species [ROS]), favor tumor growth (through the production of growth factors and neutrophil elastase [NE]), promote the remodeling of the extracellular matrix (ECM) and tumor cell invasive capabilities (through the release of proteases, transforming growth factor β [TGF-β], hepatocyte growth factor [HGF], and oncostatin M [OSM]), support angiogenesis and lymphangiogenesis (through the release of vascular endothelial growth factors [VEGFs], matrix metalloprotease (MMP)-9, and Bv8), and suppress antitumoral adaptive immunity (through arginine depletion and expression of suppressive soluble and membrane molecules, such as interleukin (IL)-10 and programmed cell death protein 1 ligand (PD-L1). See text for details. IDO, Indoleamine 2,3-dioxygenase; M-CSF, macrophage colony-stimulating factor; EGF, epidermal growth factor; Treg, regulatory T cell; IFN, interferon.
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