Abstract
It has been estimated that about 16% (1,450,000 cases) of the worldwide incidence of cancer in 1990 can be attributed to infection with either the hepatitis B and C viruses, the human papilloma viruses, Epstein-Barr virus, human T-cell lymphotropic virus I, human immunodeficiency virus (HIV), the bacterium Helicobacter pylori, schistosomes or liver flukes (Pisani et al. 1997). This estimate was made following the evaluations of the IARC monographs program, which has evaluated several infectious agents as carcinogenic to humans (IARC Working Group on the Evaluation of Carcinogenic Risks to Humans 1994a,b, 1995, 1996, 1997). Table 1 summarizes some human cancers for which infection and inflammation have been associated with increased risk. Chronic infection by a variety of viruses, bacteria, or parasites and tissue inflammation such as gastritis and hepatitis, which are often caused by chronic infection, are recognized risk factors for human cancers at various sites. Moreover, the chronic inflammation induced by chemical and physical agents such as cigarette smoke and asbestos and autoimmune and inflammatory reactions of uncertain etiology (e.g., pernicious anemia, ulcerative colitis, pancreatitis, etc.) are also associated with an increased risk of cancer. Thus a significant fraction of the global cancer burden is attributable to chronic infection and inflammation.
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Ohshima, H., Tatemichi, M. (2003). Infections, Inflammation and Cancer: Roles of Reactive Oxygen and Nitrogen Species. In: Vainio, H.U., Hietanen, E.K. (eds) Mechanisms in Carcinogenesis and Cancer Prevention. Handbook of Experimental Pharmacology, vol 156. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-08602-5_12
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