Inflammation and Cancer

Tissues impacted by chronic infiltration of immune cells, for example, chronic inflammation, have a significantly increased risk of neoplasia. Once tumor development begins, immune cells that infiltrate and subsequently reside within neoplastic microenvironments regulate paracrine pathways in the tissue that foster neoplastic cell survival and proliferation, as well as regulating vascular cells, mesenchymal support cells, and other immune cells to similarly support neoplastic progression and tumor development. We now appreciate that immune microenvironments in solid tumors are targets for anticancer therapy, whereby therapeutics aim to neutralize their tumor-promoting activities, which is coincident with bolstering their embedded activities to foster T cell mobilization and cytotoxic functions through enhanced recognition of tumor-specific antigens. The key leukocytes that contribute to acute versus chronic inflammation in cancer, as well as the mechanisms by which they do so are subjects of the ongoing investigations. This article outlines differences between acute and chronic inflammation in the context of cancer, how each state arises, and how each can be manipulated for development of new cancer therapeutics.