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(1) Background: Colorectal cancer (CRC) is among the best examples of the relationship between inflammation and increased cancer risk. (2) Methods: To examine the effects of spontaneous low-grade chronic inflammation on the pathogenesis of CRC, we developed a new murine model of colitis-associated cancer (CAC) by crossing Mucin 2 mutated mice (Winnie) with <i>Apc^Min/+</i> mice. (3) Results: The resulting Winnie-<i>Apc^Min/+</i> model combines an inflammatory background with a genetic predisposition to small intestinal polyposis. Winnie-<i>Apc^Min/+</i> mice show an early occurrence of inflammatory signs and dysplastic lesions in the distal colon with a specific molecular signature. (4) Conclusion: The Winnie-<i>Apc^Min/+</i> model is a perfect model to demonstrate that chronic inflammation represents a crucial risk factor for the onset and progression of tumoral lesions in individuals genetically predisposed to CRC.