Fig. 2.

Role of the innate immune response at different stages of tumorigenesis. Chronic inflammation can stimulate tumour initiation via the production of DNA‐damaging agents such as ROS (A). Additionally, certain oncogenes can feedback into this process by potentiating pathways in tumour cells. Myeloid cells have been shown to contribute to this process via the generation of DNA‐damaging agents. During tumour growth, tumour cells release DAMPs into the tumour microenvironment (B). Damage‐associated molecular patterns (DAMPs) can be sensed by pattern recognition receptors (PRRs) on stromal cells, causing these cells to release growth factors and inflammatory cytokines, which can promote tumour survival. Inflammatory cytokines activate NFκB in tumour cells, which can stimulate cell survival pathways. The inflammatory microenvironment can stimulate innate immune cells such as tumour‐associated macrophages (TAMs), which can feed back into the inflammatory microenvironment, whereas other innate immune cells play an antitumorigenic role such as natural killer (NK) cells and dendritic cells (DCs). The innate immune response also enhances metastasis via inflammation, which can increase epithelial‐to‐mesenchymal transition and cell migration (C).