Mechanisms coupling the hemostatic system to colitis-associated cancer.

摘要

A link between inflammation and the development of cancer is well established. Indeed, approximately 15-20% of malignancies are thought to arise secondary to chronic inflammation [1]. One of the clearest illustrations of the link between inflammation and cancer is the strong association between chronic colitis (i.e., ulcerative colitis and Crohn's disease) and colon cancer, the second leading cause of cancer deaths [2-5], The precise mechanisms coupling inflammatory processes to colon cancer progression have not been fully defined and are likely to be numerous and complex. Chronic bowel inflammation has been proposed to drive cancer initiation by increasing intestinal epithelial cell turnover, increasing the likelihood of an epithelial carcinogenic mutation. Chronic exposure of epithelial cells to inflammatory mediators, such as reactive oxygen and nitrogen species, may also lead to mutagenesis by causing DNA damage [6,7]. Additionally, local inflammation may support the proliferation of transformed epithelial cells and the development of tumor stroma through the local release of chemokines, cytokines, growth factors, and pro-angiogenic factors [8].