Notably, it was found that DEN accelerate liver tumor growth through enhanced c-met signaling loss while organic selenium delayed chemical carcinogenesis through maintaining hepatocyte growth factor receptor and improving antioxidant status of treated mice. Moreover selenium treated groups showed fewer and smaller foci and nodules than the DEN group. At the end of the experiment no mice showed hepatocellular carcinoma (HCC) in the DEN-Se group but showed only advanced dysplasia. While acontrol positive group which administered DEN showed hepatocellular carcinoma in all mice. Additionally, selenium maintained liver enzymes and antioxidant liver status to basal level while DEN enhanced significant increase of liver enzymes and significant decrease of super-oxide dismutase and glutathione levels to basal level. We conclude that selenium had an inhibitory effect on the initiation and promotion stages of DEN-induced preneoplastic foci and nodules. Selenium also prevented progression of these nodules to HCC.