Development of
tumor over many years leads to reciprocal alterations in the host immune response and the
tumor, enabling
tumor growth seemingly paradoxically in the setting of
necrosis and
inflammation. Innate immune cells, granulocytes - neutrophils, eosinophils, basophils - and mast cells belong to the first line of defense sensing pathogen and damage associated molecular pattern (
PAMPs, DAMPs) signals, initiating and modulating the subsequent inflammatory response. Nontheless, the prevailing contemporary strategies of
immunotherapy for
cancer have focused on the second line of the immune response, the adaptive immune response. We have determined that most highly evolved
tumors in adults undergo
necrosis, releasing DAMPs, promoting reactive angiogenesis, stromagenesis and reparative epithelial proliferation of the
tumor cell. Means to aerobically eliminate such DAMPs by
peroxidases released by innate immune effectors allows us to consider novel strategies for limiting
tumor progression. Summarized here is our current understanding of acute and chronic
inflammation and its impact on
tumor development, the pathophysiology of immunity in
cancer, and the influence of granulocytes and mast cells in this setting.