Editorial [ Inflammatory Bowel Disease and Inflammation-Associated Colon Cancer:Partners in Crime Guest Editor: Silvio Danese ]

Chronic inflammation makes individuals susceptible to cancer. This is true in many forms of inflammatory diseases, including Inflammatory bowel disease (IBD). The link between inflammation and the promotion of cancer was first observed in the nineteenth century, but only in recent years it has became a generally accepted phenomenon. Epidemiological studies have clearly shown that chronic inflammation predisposes individuals to certain cancers, and conversely that non-steroidal anti-inflammatory agents protects against some tumors. Most Epidemiological studies have shown that chronic inflammation predisposes individuals to certain cancers, and conversely that non-steroidal anti-inflammatory agents protect against several tumours. Most precancerous and cancerous tissues show signs of inflammation; this involves the movement of innate immune cells into the tissue, the presence of specific inflammatory signalling molecules (cytokines and chemokines), changes in tissue structure (remodelling), and the formation of new blood vessels (angiogenesis). Further studies found that cancer-associated inflammation actually promotes tumour growth and progression. For instance, innate immune cells called tumour-associated macrophages work their way into precancerous tissue, and can release factors that promote tumour growth and metastasis. Accordingly, in many human tumours, the infiltration of large numbers of these macrophages is associated with poor prognosis. Moreover, increased expression of genes associated with macrophage infiltration (such as CD68) forms part of the molecular signatures that herald poor prognosis in certain cancers. All the above described processes occur also in IBD, where it has been longly recognized a heightened risk of developing colonic cancer in both ulcerative colitis (UC) and colonic Crohn's disease (CD). For long time the association between colonic cancer and IBD has been only epidemiological. However, very recently, many of the molecular mechanisms linking the two processes have started to be clarified. In this special issue of Current Drug Target, key opinion leaders in the field of IBD and inflammation-associated colon cancer will summarize the advances in the knowledge of the pathogenesis of both forms of IBD. In the last decade, a tremendous progression in the genetic field of CD and UC has been made. This has helped to clarify some key and unexpected pathogenic events. For instance, it is now firmly established that in CD the innate immunity may play an underrated role in its pathogenesis. In addition, many of the cytokine networks and signaling molecules that mediate intestinal inflammation have been identified. This progress with the help of the biotechnology has lead to design entirely new therapeutic approaches, with the establishment of the so called biological therapies. Some of these biological therapies are now commonly used in the routine IBD clinic, and are considerably changing the natural history of both forms of IBD. Beside creating new and more specific and selective therapies, the understanding of the mechanisms that underlie intestinal inflammation and the use in the laboratory of animal models reproducing inflammation-associated colon cancer has helped in shedding light also on the steps that go from inflammation to cancer, and in identifying new therapeutic targets to avoid the progression from gut inflammation to cancer, that act as partners in crime in the intestinal scene. Abbreviations: CD, Crohn's disease; UC, ulcerative colitis; IBD, inflammatory bowel disease.