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“Background HCC is a heterogeneous disease in terms of etiology, biologic and clinical behavior. Meanwhile, hepatocarcinogenesis Guanylate cyclase 2C is a long-term, multistep process associated with changes in gene expression profiles. In the last several years, there have been important

gains in our understanding of the pathogenesis of HCC and our appreciation of the critical oncogenic and tumor suppressor pathways involved in hepatocarcinogenesis [1–5]. Despite this, current knowledge about the molecular pathogenesis of HCC is a result of investigations of fully developed HCC. Very little is known about how many genes concur at the molecular level of tumor development, progression and aggressiveness. Molecular profiling has been successfully used to identify candidate genes for HCC in human and animal model systems[3]. Although many approaches (including genome-scale studies) provide insights into some of the stages in human tumorigenesis, a sequential analysis of the development of tumors in humans is very difficult. Most of them have not given us the gene expression profiles that could point to those genes that play key roles during the whole carcinogenetic process from initiation to metastasis. Animal models of carcinogenesis have permitted the examination of the stages of neoplastic development in considerable detail. In this study, we established the rat model of liver cancer induced by DEN to explore the processes of initiation and progression of HCC[6].