The 43 patients who underwent transplant accounted for $17,025,037 of the overall costs at $395,000 per transplanted patient compared to $5,817,300 for the non transplant

patients for a mean cost of $100,299 per patient. CONCLUSIONS: Pharmaco-economic studies of HCV treatment need to model real life estimations of true direct cost of HCC care. Disclosures: Daniel Mansuri – Stock Shareholder: Gilead Sciences Nezam H. Afdhal – Consulting: Merck, Vertex, Idenix, GlaxoSmithKline, Spring-bank, Gilead, Pharmasett, Abbott; Grant/Research Support: Merck, Vertex, Ide-nix, GlaxoSmithKline, Springbank, Gilead, Pharmasett, Abbott The following people have nothing to disclose: Andreea M. Catana, Nidhi Sethi, Annie Vong, Saurabh Sethi “
“MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression by interacting with the 3′ untranslated region (3′-UTR) of multiple mRNAs. Recent studies have linked miRNAs to the development of cancer metastasis. In this study, we show find more that miR-194 is specifically expressed in the human gastrointestinal tract and kidney. Moreover, miR-194 is highly expressed in hepatic epithelial cells, but not in Kupffer cells or hepatic stellate cells, two

types of mesenchymal cells in the liver. miR-194 expression was decreased in hepatocytes cultured in vitro, which had undergone a dedifferentiation process. Furthermore, selleck chemicals expression of miR-194 was low in liver mesenchymal-like cancer cell lines. The overexpression of miR-194 in liver mesenchymal-like cancer cells reduced the expression of the mesenchymal cell marker N-cadherin

and suppressed invasion and migration of the mesenchymal-like cancer cells both in vitro and in vivo. We further demonstrated that miR-194 targeted the 3′-UTRs of several genes that were involved in epithelial-mesenchymal transition and cancer metastasis. Conclusion: These results support a role of miR-194, mafosfamide which is specifically expressed in liver parenchymal cells, in preventing liver cancer cell metastasis. (HEPATOLOGY 2010;.) The liver is the central organ of metabolism in mammals, controlling energy equilibrium, synthesizing plasma proteins and bile acids, and detoxifying metabolic wastes and xenobiotics. Hepatocytes, the parenchymal cells of the liver, make up more than 80% of liver mass and form its epithelial layer.1 The transformation of hepatocytes following chronic injury, induced by viral infection or alcohol abuse, leads to hepatocellular carcinoma (HCC). The long-term survival of HCC patients is unsatisfactory due to a high incidence of recurrence and metastasis after tumor resection, with a 5-year actuarial recurrence rate of 75%-100%.2 Emerging evidence indicates that aberrant activation of epithelial-mesenchymal transition (EMT) is an early step in cancer metastasis.3 EMT is characterized by loss of cell adhesion, down-regulation of the epithelial gatekeeper protein E-cadherin, and up-regulation of N-cadherin and vimentin, two mesenchymal cell markers.