Biology of Inflammation and Cancer

Epidemiological evidence points to a connection between long-term inflammation and the development of cancer that is characterized by dysplasia, hyperplasia, and sometimes irreversible cancer transformations. Nearly 15% of worldwide cancer incidence in humans is associated with microbial infection (Kuper et al. 2002). Chronic infections, with human papilloma virus or with hepatitis B or C viruses in immunocompetent human hosts, can lead to cervical and hepatocellular carcinomas, respectively. Infection with the human herpes virus can produce Kaposi s sarcoma in the skin. Karposi s cancers are seen more often in the IDS-compromised AIDS patients. After protracted inflammation, Helicobacter pylori can cause stomach irrita- 

Chronic inflammatory states associated with infection or xenobiotic chemical exposure from the environment can produce genomic lesions that, in time, can become initiated tumors. It is known that hosts do fight microbial infections by moderate production of various free radicals reactive oxygen species (ROS) [e.g., hydroxyl radical (OH ) and the superoxide radical (OT)] or reactive nitrogen species (RNS) [e.g., nitric oxide (NO ) and the strong oxidant, peroxynitrite (ONOO )]. Within limits inflammatory signaling pathways of the host can control excessive free radical concentrations by means of enzymes such as NADPH oxidase, myeloperoxidase, nitric oxide synthase, and others (Federico et al. 2007 Rakoff-Nahonm 2006). 

the premalignant early I-stage tumors are wound-like (Coussens and Werb 2002). The known cancer stages were reviewed in Section 5.2. In many ways, 

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