The tumor microenvironment is a complex framework, in which myeloid cells play important roles in sculpting cancer development from tumor initiation to metastasis. Immune cells are key participants of the tumor microenvironment where they can promote or inhibit cancer formation and development. Plasticity is a widely accepted hallmark of myeloid cells and in particular of the monocyte-macrophage lineage. It includes the ability to display a wide spectrum of activation states in response to distinct signals and classical M1 or alternative M2 macrophages represent a paradigm of this feature. Neutrophils have long been viewed as terminally differentiated effector cells, playing a major role during the acute phase of inflammation and resistance against microbes. Recent evidence questioned this limited point of view, indicating that neutrophils can interact with distinct cell populations and produce a wide number of cytokines and effector molecules. Therefore, macrophages and neutrophils are both integrated in the regulation of the innate and adaptive immune responses in various inflammatory situations, including cancer.
Keywords: CRC; Cancer; ECM; HCC; HNSCC; Inflammation; MDSC; MMP; Macrophages; Neutrophils; TAM; TAN; TEN; VEGF; colorectal cancer; extracellular matrix; head and neck squamous cellular cancer; hepatocellular carcinoma; matrix metalloproteases; myeloid derived suppressor cells; tumor associate neutrophils; tumor associated macrophages; tumor entrained neutrophils; vascular endothelial growth factor.
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