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- W2080178481 abstract "We previously described a mouse model of ulcerative colitis linked to T-bet deficiency in the innate immune system. Here, we report that the majority of T-bet−/−RAG2−/− ulcerative colitis (TRUC) mice spontaneously progress to colonic dysplasia and rectal adenocarcinoma solely as a consequence of MyD88-independent intestinal inflammation. Dendritic cells (DCs) are necessary cellular effectors for a proinflammatory program that is carcinogenic. Whereas these malignancies arise in the setting of a complex inflammatory environment, restoration of T-bet selectively in DCs was sufficient to reduce colonic inflammation and prevent the development of neoplasia. TRUC colitis-associated colorectal cancer resembles the human disease and provides ample opportunity to probe how inflammation drives colorectal cancer development and to test preventative and therapeutic strategies preclinically." @default.
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- W2080178481 date "2009-09-01" @default.
- W2080178481 modified "2023-09-25" @default.
- W2080178481 title "Colitis-Associated Colorectal Cancer Driven by T-bet Deficiency in Dendritic Cells" @default.
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- W2080178481 doi "https://doi.org/10.1016/j.ccr.2009.07.015" @default.
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