**1. Introduction**

Cancer is a pro-inflammatory disease. The link between inflammation and cancer was first noticed over 150 years ago. In 1863, Virchow observed that tumours tend to occur at sites of chronic inflammation (Balkwill, 2001).

Epidemiological studies have recently emerged which support the association between cancer and inflammation. Viruses and bacteria cause chronic inflammation and are significant risk factors in the development of malignancy. Human papilloma viruses, hepatitis B, hepatitis C and helicobacter pylori are well studied examples of this phenomenon which result in cervical cancer, hepatocellular cancer, lympho-proliferative disorders and gastric cancer respectively. Furthermore, increased risk of malignancy is associated with chronic inflammation caused by chemical and physical agents (Gulumian, 1999). In addition to epidemiological data, gene-cluster polymorphisms that lead to increased levels of pro-inflammatory cytokine release are associated with a poorer prognosis and disease severity in cancer patients (Warzocha, 1998; El-Omar, 2000). Moreover, the fact that chronic use of NSAIDs, such as aspirin are shown to reduce the incidence of numerous cancer types including colon, lung and stomach, gives additional supporting evidence for the link between inflammation and cancer (Wang, 2003).
