Journal
CANCER CELL
Volume 17, Issue 2, Pages 135-147Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2009.12.041
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Funding
- National Cancer Institute
- Irving Institute Fellowship Program of the Cancer Research Institute
- NCI [T32 CA09043]
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Cancer-associated fibroblasts (CAFs) support tumorigenesis by stimulating angiogenesis, cancer cell proliferation, and invasion. We demonstrate that CAFs also mediate tumor-enhancing inflammation. Using a mouse model of squamous skin carcinogenesis, we found a proinflammatory gene signature in CAFs isolated from dysplastic skin. This signature was maintained in CAFs from subsequent skin carcinomas and was evident in mammary and pancreatic tumors in mice and in cognate human cancers. The inflammatory signature was already activated in CAFs isolated from the initial hyperplastic stage in multistep skin tumorigenesis. CAFs from this pathway promoted macrophage recruitment, neovascularization, and tumor growth, activities that are abolished when NF-kappa B signaling was inhibited. Additionally, we show that normal dermal fibroblasts can be educated by carcinoma cells to express proinflammatory genes.
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