The process of inflammation has a paradoxical effect. This is mostly due to the metabolic responses triggered by the release of the three proinflammatory cytokines, interleukin 1β (IL-1β), tumour necrosis factor α (TNF-α), and interleukin 6 (IL-6). As an integral part of the body’s response to infection and injury, these mediators release substrate, from host tissues, to support T and B lymphocyte activity, create a hostile environment for invading pathogens, via a raised body temperature and oxidant production, and initiate downregulation of the process once invasion has been defeated.¹ All of these metabolic effects come at considerable cost to the host, as witnessed by the extensive tissue depletion, anorexia, and anaemia seen in severely infected and injured patients.² However, the cost is of great biological value if recovery from infection and injury are achieved. The inflammatory process contains elements which inherently upregulate the response. Oxidants will increase proinflammatory cytokine production by activating nuclear factor κB (NFκB). A wide range of genes associated with the inflammatory process have NFκB response elements in their structure. These include genes for proinflammatory cytokines and adhesion molecules.¹

Tumour cells may initiate the inflammatory response as effectively as invading pathogens. However, while the inflammatory process may be effective in dealing with single malignant cells, once cancer is established the inflammatory process becomes a cause of the patient’s demise, rather than a means of destroying the tumour. In addition to stimulating the cytokine mediated and hormonal aspects of the inflammatory response, tumour specific products …