Inflammation, Microenvironment, and the Immune System in Cancer Progression

Abstract

Since Virchow first proposed in 1863 that tumors could originate from sites of chronic inflammation, it has been well established that chronic inflammation both contributes to cancer progression and predisposes tissue to various types of cancer. Experimental, clinical, and epidemiological studies have all demonstrated the strong association between chronic inflammation and cancer, and many studies have correlated the prolonged presence of the inflammatory milieu with an increased risk for developing cancer. Proinflammatory cytokines, chemokines and adhesion molecules, which regulate the sequential recruitment of leukocytes, are frequently observed in tumor microenvironment. These early desmoplastic changes could stimulate fibroblasts and endothelial cell division and produce components for tissue remodeling and neovascularization, ultimately promoting neoplastic processes. In this review article we overview the current understanding of the role of chronic inflammation in neoangiogenesis, tumor initiation, promotion, and progression.

The Indispensable Role of CCR5 for In Vivo Suppressor Function of Tumor-Derived CD103+ Effector/Memory Regulatory T Cells

“…These data were consistent with previous observations that CD103 + Tregs had the preferential migration into inflamed sites for suppression of inflammatory reactions in murine models of graft-versus-host disease and autoimmune arthritis (4,6). The tumor microenvironment had been deemed as an unresolved chronic inflammation that was important for the immune evasion of the tumor (17)(18)(19)(20). Therefore, the preferential migration capacity of CD103 + Tregs into inflamed tissue could be the reason for the accumulation of CD103 + Tregs in the tumor microenvironment, an unresolved chronic inflammation.…”

NSAID analgesic ketorolac used perioperatively may suppress early breast cancer relapse: particular relevance to triple negative subgroup

“…Since Virchow first proposed in 1863 that tumors could originate from sites of chronic inflammation, it has been well established that chronic inflammation both contributes to cancer progression and predisposes tissue to various types of primary and metastatic cancer [6].…”

Unconventional Causes of Conventional Oral Cancer

“…The mechanism by which CTOM is thought to contribute to carcinogenesis is not clearly identified. It has been proposed that the wound of the oral mucosa may facilitate the absorption of other chemical carcinogens [33].…”