An association between inflammation and cancer has already been noted in the 19th century (Balkwill and Mantovani, 2001), and more recent epidemiological data had led to the estimate that at least 20% of cancer deaths are linked to chronic infections and persistent inflammation (Kuper et al., 2000). Notable examples are gastric cancer and Helicobacter pylori infections (Roder, 2002), hepatocellular carcinoma (HCC) and viral hepatitis (Fattovich et al., 2004), and colitis-associated cancer (CAC)(Ekbom, 1998). However, epidemiological associations do not establish causality, and the mechanisms that link inflammation and cancer have only been addressed recently. Initial work in this area had demonstrated the requirement of tumor necrosis factor (TNF)-α and signaling via the type I TNF-α receptor (TNFR1) in the development of squamous cell carcinoma (SCC) induced by the classical two-stage carcinogenesis protocol (Moore et al., 1999). The molecular mechanism by which TNFR1 signaling promotes tumor development, however, has not been thoroughly explored, although it is thought to be mediated via protein kinase C (PKC) α and activator protein 1 (AP-1) transcription factors (Arnott et al., 2002). Another cytokine, colony stimulating factor-1 (CSF-1), was shown to be required for progression of fully malignant mammary carcinoma in mice, presumably through its effect on macrophage development (Lin et al., 2001). The mechanisms by which macrophages stimulate the development and progression of mammary carcinoma are still being