Breast cancer is one of the leading causes of cancer related mortality in women in the western world and inflammation is correlated with bad prognosis in breast cancer. Breast tumors are characterized by an extensive desmoplastic stroma, abundantly populated by fibroblasts. Cancer Associated Fibroblasts (CAFs) have been shown to promote the growth of mammary tumors by directly stimulating tumor cell proliferation and by enhancing angiogenesis, but their role in mediating inflammation in breast tumorigenesis is unknown. Despite the fact that most of cancer-related mortality is a result of tumor metastasis, and not of the primary tumor, very little is known to date about the role of the metastatic stroma in allowing disseminated tumor cells from the primary tumor to propagate and colonize the metastatic organ. Even less is known about the role of fibroblasts in this critical stage of the metastatic cascade. Using a genetically engineered mouse model of mammary carcinoma we will investigate pro-inflammatory signaling by CAFs during different stages of mammary tumorigenesis, starting at early hyperplastic lesions, elucidate its functional importance and define the molecular pathways that underlie inflammatory signaling by mammary CAFs in tumor progression and metastasis.
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