Chronic inflammation mediates tumor development by promoting a constant influx of inflammatory cells capable of modulating genes involved in cancerogenesis and creating micro and macroenvironments that support cancer growth. A major side effects of cancer inflammation is the pathological expansion and recruitment of myeloid cells endowed with immunosuppressive activity, to control the unresolved inflammation. Tumors reprogram myeloid cell differentiation and functions through various mechanisms, including altered metabolism, cancer-related inflammation andalteration of the hematopoietic output. These events govern the expansion of myeloid suppressor populations, mainly myeloid-derived suppressor cells (MDSCs) and tumor associated macrophages (TAMs). MDSCs and TAMs orchestrate tumor immunosuppression in concert with regulatory T cells, inhibitory cytokines and immune check points receptors, and act to subvert anti-tumor immunity, hence causing that eventually support immune evasion establishing a bottleneck for cancer immunotherapy. I will discuss inflammatory circuits and epigenetic events sustaining the expansion and the tumor-promoting reprogramming of myeloid cells in cancer bearers.
Disclosure of Interest None declared