Journal
CANCER CELL
Volume 16, Issue 3, Pages 208-219Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2009.07.015
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Funding
- National Institutes of Health [CA112663]
- Ellison Scholar
- Damon Runyon Cancer Research Foundation
- Burroughs Wellcome Career in Medical Sciences
- V Foundation
- DF/HCC [GI SPORE 1P50CA127003-02]
- Irving Janock
- HDDC Pilot
- MRC [G0802068] Funding Source: UKRI
- Medical Research Council [G0600698B, G0802068] Funding Source: researchfish
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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.
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