Pathology Research International [36] M. Chuma, M. Sakamoto, K. Yamazaki et al., “Expression proﬁling in multistage hepatocarcinogenesis: identiﬁcation of HSP70 as a molecular marker of early hepatocellular carcinoma,” Hepatology, vol. 37, no. 1, pp. 198–207, 2003. [37] P. Kaposi-Novak, I. Libbrecht, HG. Woo et al., “Central role of c-Myc during malignant conversion in human hep- atoeareinogenesis,” Cancer Research, vol. 69, no. 8, pp. 2775– 2782, 2009. [38] H. C. Hsu, W. Cheng, and PO. L. Lai, “Cloning and expression of a developmentally regulated transcript MXR7 in hepatocellular carcinoma: biological signiﬁcance and temporospatial distribution,” Cancer Research, vol. 57, no. 22, pp. 5179–5184, 1997. [39] N. Yamauchi, A. Watanabe, M. Hishinuma et al., “The glypican 3 oncofetal protein is a promising diagnostic marker for hepatocellular carcinoma,” Modern Pathology, vol. 18, no. 12, pp. 1591–1598, 2005. [40] L. Di Tommaso, G. Franchi, N. P. Young et al., “Diagnostic value of HSP70, glypican 3, and glutamine synthetase in hepatocellular nodules in cirrhosis,” Hepatology, vol. 45, no. 3, pp. 725–734, 2007. [41] A. Cadoret, C. Ovejero, B. Terris et al., “New targets of β- catenin signaling in the liver are involved in the glutamine metabolism,” Oncogene, vol. 21, no. 54, pp. 8293–8301, 2002. [42] L. Christa, M. T. Simon, J. P. Flinois, R. Gebhardt, C. Brechot, and C. Lasserre, “Overexpression of glutamine synthetase in human primary liver cancer,” Gastroenterology, vol. 106, no. 5, pp. 1312–1320, 1994. [43] L. Di Tommaso, A. Destro, J. Y. Seok et al., “The application of markers (HSP70 GPC3 and GS) in liver biopsies is useful for detection of hepatocellular carcinoma,” Journal of Hepatology, vol. 50, no. 4, pp. 746–754, 2009. [44] T. Roskams and M. Kojiro, “Pathology of early hepatocellular carcinoma: conventional and molecular diagnosis,” Seminars in Liver Disease, vol. 30, no. 1, pp. 17–25, 2010. [45] A. S. Adler, M. Lin, H. Horlings, D. S. A. Nuyten, M. J. Van De Vijver, and H. Y. Chang, “Genetic regulators of large-scale transcriptional signatures in cancer,” Nature Genetics, vol. 38, no. 4, pp. 421–430, 2006. [46] F. Trevisani, M. Frigerio, V. Santi, A. Grignaschi, and M. Bernardi, “Hepatocellular carcinoma in non-cirrhotic liver: a reappraisal,” Digestive and Liver Disease, vol. 42, no. 5, pp. 341–347, 2010. [47] M. F. Madhoun, J. Fazili, B. C. Bright, T. Bader, D. N. Roberts, and M. S. Bronze, “Hepatitis C prevalence in patients with hepatocellular carcinoma without cirrhosis,” American Journal of the Medical Sciences, vol. 339, no. 2, pp. 169–173, 2010. [48] Y. Takuma and K. Nouso, “Nonalcoholic steatohepatitis- associated hepatocellular carcinoma: our case series and literature review,” World Journal of Gastroenterology, vol. 16, no. 12, pp. 1436–1441, 2010. [49] S. Liu, K. W. Chan, B. Wang, and L. Qiao, “Fibrolamellar hep- atocellular carcinoma,” American Journal of Gastroenterology, vol. 104, no. 10, pp. 2617–2624, 2009. [50] H. M. Ross, H. D.J. Daniel, P. Vivekanandan et al., “Fibrolamellar carcinomas are positive for CD68,” Modern Pathology, vol. 24, no. 3, pp. 390–395, 2011. [51] J. M. Llovet, A. M. Di Bisceglie, J. Bruix et al., “Design and endpoints of clinical trials in hepatocellular carcinoma,” Journal of the National Cancer Institute, vol. 100, no. 10, pp. 698–711, 2008. 13 [52] Q. H. Ye, L. X. Qin, M. Forgues et al., “Predicting hepatitis B virus-positive metastatic hepatocellular carcinomas using gene expression proﬁling and supervised machine learning,” Nature Medicine, vol. 9, no. 4, pp. 416–423, 2003. [53] A. Forner, M. E. Reig, C. Rodriguez De Lope, and J. Bruix, “Current strategy for staging and treatment: the BCLC update and future prospects,” Seminars in Liver Disease, vol. 30, no. 1, pp. 61–74, 2010. [54] H. Huynh, “Molecularly targeted therapy in hepatocellu- lar carcinoma,” Biochemical Pharmacology, vol. 80, no. 5, pp. 550–560, 2010. [55] N. Nishida, T. Nishimura, T. Ito, T. Komeda, Y. Fukuda, and K. Nakao, “Chromosomal instability and human hepatocar- cinogenesis,” Histology and Histopathology, vol. 18, no. 3, pp. 897–909, 2003. [56] Y. Midorikawa, W. Tang, and Y. Sugiyama, “High-resolution mapping of copy number aberrations and identiﬁcation of target genes in hepatocellular carcinoma,” Bioscience Trends, vol. 1, no. 1, pp. 26–32, 2007. [57] M. A. Patil, I. Gu¨tgemann, J. Zhang et al., “Array-based comparative genomic hybridization reveals recurrent chro- mosomal aberrations and Jab1 as a potential target for 8q gain in hepatocellular carcinoma,” Carcinogenesis, vol. 26, no. 12, pp. 2050–2057, 2005. [58] H. Katoh, H. Ojima, A. Kokubu et al., “Genetically dis- tinct and clinically relevant classiﬁcation of hepatocellular carcinoma: putative therapeutic targets,” Gastroenterology, vol. 133, no. 5, pp. 1475–1486, 2007. [59] D. Y. Chiang, A. Villanueva, Y. Hoshida et al., “Focal gains of VEGFA and molecular classiﬁcation of hepatocellular carcinoma,” Cancer Research, vol. 68, no. 16, pp. 6779–6788, 2008. [60] J. W. Marsh, S. D. Finkelstein, A. J. Demetris et al., “Genotyping of hepatocellular carcinoma in liver transplant recipients adds predictive power for determining recurrence- free survival,” Liver Transplantation, vol. 9, no. 7, pp. 664– 671, 2003. [61] I. Dvorchik, M. Schwartz, M. I. Fiel, S. D. Finkelstein, and J. W. Marsh, “Fractional allelic imbalance could allow for the development of an equitable transplant selection policy for patients with hepatocellular carcinoma,” Liver Transplantation, vol. 14, no. 4, pp. 443–450, 2008. [62] C. Schmidt and J. W. Marsh, “Molecular signature for HCC: role in predicting outcomes after liver transplant and selection for potential adjuvant treatment,” Current Opinion in Organ Transplantation, vol. 15, no. 3, pp. 277–282, 2010. [63] M. Schwartz, I. Dvorchik, S. Roayaie et al., “Liver transplan- tation for hepatocellular carcinoma: extension of indications based on molecular markers,” Journal of Hepatology, vol. 49, no. 4, pp. 581–588, 2008. [64] S. Imbeaud, Y. Ladeiro, and J. Zucman-Rossi, “Identiﬁcation of novel oncogenes and tumor suppressors in hepatocellular carcinoma,” Seminars in Liver Disease, vol. 30, no. 1, pp. 75– 86, 2010. [65] P. Laurent-Puig, P. Legoix, O. Bluteau et al., “Genetic alterations associated with hepatocellular carcinomas deﬁne distinct pathways of hepatocarcinogenesis,” Gastroenterology, vol. 120, no. 7, pp. 1763–1773, 2001. [66] V. Audard, G. Grimber, C. Elie et al., “Cholestasis is a marker for hepatocellular carcinomas displaying β-catenin mutations,” Journal of Pathology, vol. 212, no. 3, pp. 345–352, 2007.