Abstract
Abstract Most gastrointestinal cancers arise in the setting of chronic inflammation, but which leads to the recruitment of additional stromal cells, but the nature of these cells have not been well-defined. Carcinoma-associated fibroblasts (CAFs) that express alpha-smooth-muscle-actin (αSMA+) are thought to contribute to cancer progression but their precise origin has not been established. We have employed IL-1β transgenic mice and Helicobacter felis-infected mice that develop gastric dysplasia and cancer to investigate the origins and contributions of CAFs. These studies suggest that chronic inflammation of the GI tract, along with other carcinogenic stimuli, results in remodeling of the bone marrow and recruitment of bone marrow-derived cells to the incipient cancer site. At least 20% of CAFs originate from BM cells, and BM-derived CAFs promote tumor growth in organotypic and xenograft models. Thus, BM-derived fibroblastic cells create a new cancer niche that contributes to the progression of cancer, and as such represent a potential target for cancer prevention therapy. Citation Information: Cancer Prev Res 2010;3(12 Suppl):CN12-04.
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