Dynamics of inflammatory signals within the tumor microenvironment

Figure 3 Molecular pathways of chronic inflammation leading to tumorigenesis. Genetic mutations trigger tumor development. The immune system attempts to perform immunosurveillance by identifying and eliminating transformed cells, but this fails as cancer progresses. During tumorigenesis and chronic inflammation, the pathogens such as bacteria and viruses interact with toll-like receptors triggering nuclear factor kappa-B signaling produces proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1, IL-6 and other chemokines. IL-1 production mediates recruitment of inflammatory cells and synthesis of reactive oxygen species leading to genetic mutations and DNA damage. Additionally, chronic inflammation aids in epithelial-to-mesenchymal transition that enhances the tumor development. EMT: Epithelial-to-mesenchymal transition; IL: Interleukin; NF-кB: Nuclear factor kappa-B; ROS: reactive oxygen species; TNF-α: Tumor necrosis factor-alpha.