Inflammation in the molecular pathogenesis of cancer and atherosclerosis.

Chronic inflammation, atherosclerosis and cancer are leading causes of death in industrialized society. Epidemiological studies have shown that chronic inflammation predisposes individuals to certain cancers, while anti-inflammatory and anti-oxidant agents may protect against cancer development and metastasis. Inflammation supports the different phases of cancer development through the inflammatory molecules produced by infiltrating immune cells, resident stromal cells and even cancer cells. Although atherosclerosis has been considered to be multi-factorial disease, in which genetic and environmental factors have been implicated, inflammation also significantly contributes to plaque formation and progression, and to stenosis of atherosclerotic lesions. Major nuclear transcription factors and molecular mediators of inflammation that induce altered cell expression of adhesion molecules, proteases, and growth factors are common factors in the microenvironment leading to disease development and progression of both atherosclerosis and cancer. Important pathogenic pathways on atherosclerosis and cancer follow endothelial cell dysfunction and the activation of the hemostatic system and angiogenesis via inflammation-dependent mechanisms represent important features of this dysfunction. Therefore, novel target-oriented therapies affecting altered mechanisms of inflammation, angiogenesis and tissue proliferation may similarly inhibit atherosclerosis and cancer. Main treatment strategies include reducing oxidative stress; inhibiting chemokine, cytokine, and growth factor cell signal transmit; down-regulating excess matrix digestion; inactivating nuclear factor-kappa B signal pathway, and interfering with cell cycle regulation.