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Supplementary Figure 1. Reversion of the core transcriptional programming of HCC cells by selected drugs. In A and B, gene set enrichment analysis (GSEA) of the induced genes (upper panels) and the repressed genes (lower panels) from the 935-gene HCC signature in the gene expression profiles of the SNU387 and HepG2/C3A cell lines. A, GSEA from the gene profiles of SNU-387 (left 2 panels) and HepG2/C3A (right 2 panels) cells treated with DMSO or vorinostat. B, GSEA from the gene profiles of HepG2/C3A cells treated with DMSO or Sorafenib (left 2 panels) or Resveratrol (right 2 panels). Positive and negative enrichment scores (ES) were determined by GSEA. DMSO, dimethyl sulfoxide; HCC, hepatocellular carcinoma. Supplementary Figure 2. Four-way Venn diagram comparing gene sets included in S1, S2 and S3 HCC subtype signatures from Hoshida’s study [1] and our core HCC signature. Supporting the specificity of the gene signatures in both Hoshida’s study and our study, there was almost no overlap between the S1-3 subtype signatures and our core HCC signature. Indeed, 82% genes included in our core HCC signature were unique while only 3%, 2% and 13% genes overlapped with the S1, S2 and S3 signatures, respectively. In addition, most of genes that overlap with the S3 signature were metabolism-associated genes that were shown to be relatively up-regulated in S3-HCC, as compared to poorly differentiated HCC of S1 and S2 subtypes [1]. However, regardless of HCC subtypes, most of these genes remain commonly repressed when compared to the surrounding nontumor tissues, as observed in our core HCC signature. This comparison suggests that our core signature constitutes a unique and specific fingerprint of recurrent and common transcriptional alterations in HCC. [1] Hoshida Y, Nijman SM, Kobayashi M, Chan JA, Brunet JP, Chiang DY, Villanueva A, Newell P, Ikeda K, Hashimoto M, Watanabe G, Gabriel S, Friedman SL, Kumada H, Llovet JM, Golub TR. Integrative transcriptome analysis reveals common molecular subclasses of human hepatocellular carcinoma. Cancer Res. 2009;69(18):7385-92. PubMed PMID: 19723656.