“…Two pathways have been schematically identified as the connection between initiation of cancer and inflammation, as intrinsic pathway and extrinsic pathway. In the intrinsic pathway, internal genetic events which cause neoplasia, at the same time, would trigger the expression of inflammation-related programs and then guide the construction of an Factors Biological activity IL-1 Elevated level in patient with leukoplakia and oral cancer [71]; Inducing chemical carcigenesis of fibrosarcomas, in vivo [72]; host derived or exogenous IL-1 enhancing tumor invasiveness and metastasis, in vitro and in vivo [73] IL-6 Involved in tumor progression, such as in multiple myeloma, plasmacytomas, intestinal cancer, in vitro and in vivo, mainly through NF-κB and STAT3 [74]; Elevated IL-6 level be correlated with HCC, in vivo experiment and in clinical [75,76]; Elevated level in patient with leukoplakia and oral cancer [71] IL-23 Elevated in intestinal polyps and colorectal carcinoma [77] IFNEnhancing the antitumor activity of alveolar macrophages, in vitro [78] TNFElevated level in patient with leukoplakia and oral cancer [71] LXs Inhibiting the tumor growth of transplanted H22 in mice, in vitro and in vivo [79]; inhibiting hepatocyte growth factor-induced invasion of human hepatoma cells, in vitro [80] There is also close connection between inflammation and metastasis. A successful establishment of a metastatic lesion depends on both intrinsic properties of the tumor cells and factors derived from the tumor microenvironment that often contains secretory products of immune cells such as IL-1, IL-6, TNF and RANKL.…”