Inflammation and cancer: a failure of resolution?
There are clear links between chronic inflammation and cancer; strong epidemiological and genetic evidence indicates that inflammation can drive tumour progression, and more-recent evidence indicates that the disruption of endogenous anti-inflammatory mechanisms in mice can lead to tumour development. The resolution of inflammation is an active coordinated process that requires the production of anti-inflammatory mediators, the termination of proinflammatory signalling pathways and the appropriate clearance or migration of inflammatory cells. Disruption of any of these processes can lead to chronic persistent inflammation and tumour growth. Although the mediators and mechanisms that drive inflammation have become increasingly well characterized, the endogenous mechanisms that limit the inflammatory response, and particularly their role in cancer, are unclear. There are clear opportunities for drug discovery and the development of new therapeutic approaches that target tumour-associated inflammation and the mechanisms of chronic inflammation.
Lawrence
Toby
T
Faculty of Medicine, Imperial College, 1 Aspenlea Road, London W6 8LH, UK. t.lawrence@qmul.ac.uk
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D016753:Interleukin-10 / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009369:Neoplasms / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000276:immunology
D016212:Transforming Growth Factor beta; D016753:Interleukin-10