In the present study, a rat model of liver www.selleckchem.com/products/ganetespib-sta-9090.html cancer was established. We have listed the deregulated expression genes in the process from cirrhosis to liver cancer in the DEN-treated rat model. As indicated in the literature, this model shows that cirrhosis is a precancerous lesion of the liver. Although we only discuss some parts of the great quantity of information in this study, much unknown information remains. Functional analysis of these genes revealed discrete expression clusters, including cell proliferation, protein synthesis, and hepatocyte-specific functions. We still need to discern the key genes playing core roles in the promotion and progression of liver cancer. In this article,

we focused our attention on the global molecular events selleck that occurred in DEN-treated rats (and probably represent the earliest ones that start the multistep process of hepatocarcinogenesis). Additional information may be mined from this and similar studies to provide clues to many areas including the very important search for

diagnostic markers, therapy targets and prognosis prediction markers. Acknowledgements This study was supported by a grant from the Science Foundation of the Ministry of Health of China (No. selleck chemical wkj2004 -2-12). The authors thanks for technician Yuhua Li for assistance with preparation of tissue slices. We would like to thank Shanghai Biochip Co., Ltd. And the National Engineering Center for Biochip at Shanghai for the operation of the Affymetrix genechips. Electronic supplementary material Additional file 1: The list of deregulated DEGs sharing from cirrhosis to metastasis stage compared with control. A table for all the screened DEGs sharing from stage of liver cirrhosis

to Montelukast Sodium metastasis. (PDF 52 KB) Additional file 2: The up-regulated DEGs sharing from cirrhosis to metastasis sorted out by the following GO function. for the screened DEGs sharing from stage of liver cirrhosis to metastasis sorted out by the GO words: angiogenesis, apoptosis, cell adhesion, cell migration, cell proliferation and extracellular matrix. (PDF 46 KB) References 1. Thorgeirsson SS, Grisham JW: Molecular pathogenesis of human hepatocellular carcinoma. Nat Genet 2002, 31: 339–346.CrossRefPubMed 2. Nagai H, Pineau P, Tiollais P, Buendia MA, Dejean A: Comprehensive allelotyping of human hepatocellular carcinoma. Oncogene 1997, 14: 2927–2933.CrossRefPubMed 3. Lee JS, Grisham JW, Thorgeirsson SS: Comparative functional genomics for identifying models of human cancer. Carcinogenesis 2005, 26: 1013–1020.CrossRefPubMed 4. Zender L, Xue W, Zuber J, Semighini CP, Krasnitz A, Ma B, Zender P, Kubicka S, Luk JM, Schirmacher P, McCombie WR, Wigler M, Hicks J, Hannon GJ, Powers S, Lowe SW: An oncogenomics-based in vivo RNAi screen identifies tumor suppressors in liver cancer. Cell 2008, 13: 852–864.CrossRef 5.