Can interruption of innate immune recognition-mediated emergency myelopoiesis impede tumor progression?

Cancer cells survive and grow despite various advanced anti-cancer therapy. To overcome this antineoplastic resistance, adjuvant therapy is often required to prevent cancer cells' immunoescape capacity. Established tumors build a stressful and hostile microenvironment in order to escape protective innate and adaptive immune responses. Specific conditions and factors within tumors, including hypoxia, nutrient starvation, acidic pH, and increased levels of free radicals, provoke a state of "endoplasmic reticulum stress" in both malignant cells and infiltrating myeloid cells. The stimulated endoplasmic reticulum stress can affect cancer progression via cross-talks with the innate immune system. Recently, the immunosuppressive activities of myeloid cells in the development of antineoplastic resistance are gaining more attention. Based on all these available data, we hypothesize that interruption of innate-immune recognition-mediated emergency myelopoiesis may be beneficial in halting cancer progression.