Colorectal cancer represents a life-threatening complication of inflammatory bowel diseases. Statistics indicate that the risk to develop colorectal cancer is higher in patients affected by ulcerative colitis and to a lesser extent by Crohn's disease and that such a risk is directly proportional to the number of years of active disease. These observations suggest that chronic inflammation may substantially contribute to cancer development. However the molecular mechanisms underlying this process have been only recently started to be clarified. Indeed from the initial concept that the release of free radicals during inflammation might induce the accumulation of genetic mutations thus leading to the onset of dysplastic cells, it is now becoming clear that the large amount of cytokines and growth factors released during inflammation by immune and non immune cells may influence the carcinogenesis process. IL-6 and IL-23, cytokines which play key roles in the induction and maintenance of gut inflammation during IBDs, have been recently shown to influence the development and growth of colitis associated colorectal cancer. Moreover, the activation of the nuclear factor k B (NFkB), a transcription factor activated by several cytokines released during inflammation and responsible for many of their proinflammatory effects, have been shown to promote the growth of the colon tumors in experimental models. © 2008 Bentham Science Publishers Ltd.

Fantini M.C., P.F. (2008). Cytokines: From gut inflammation to colorectal cancer. CURRENT DRUG TARGETS, 9(5), 375-380 [10.2174/138945008784221206].

Cytokines: From gut inflammation to colorectal cancer

FANTINI, MASSIMO CLAUDIO;PALLONE, FRANCESCO
2008

Abstract

Colorectal cancer represents a life-threatening complication of inflammatory bowel diseases. Statistics indicate that the risk to develop colorectal cancer is higher in patients affected by ulcerative colitis and to a lesser extent by Crohn's disease and that such a risk is directly proportional to the number of years of active disease. These observations suggest that chronic inflammation may substantially contribute to cancer development. However the molecular mechanisms underlying this process have been only recently started to be clarified. Indeed from the initial concept that the release of free radicals during inflammation might induce the accumulation of genetic mutations thus leading to the onset of dysplastic cells, it is now becoming clear that the large amount of cytokines and growth factors released during inflammation by immune and non immune cells may influence the carcinogenesis process. IL-6 and IL-23, cytokines which play key roles in the induction and maintenance of gut inflammation during IBDs, have been recently shown to influence the development and growth of colitis associated colorectal cancer. Moreover, the activation of the nuclear factor k B (NFkB), a transcription factor activated by several cytokines released during inflammation and responsible for many of their proinflammatory effects, have been shown to promote the growth of the colon tumors in experimental models. © 2008 Bentham Science Publishers Ltd.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/12 - Gastroenterologia
English
Colitis; Colorectal cancer; IBD; IL-23; IL-6; NF-kB
Fantini M.C., P.F. (2008). Cytokines: From gut inflammation to colorectal cancer. CURRENT DRUG TARGETS, 9(5), 375-380 [10.2174/138945008784221206].
Fantini, Mc; Pallone, F
Articolo su rivista
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/28729
Citazioni
  • ???jsp.display-item.citation.pmc??? 60
  • Scopus ND
  • ???jsp.display-item.citation.isi??? 126
social impact