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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThe main risk factors for hepatocellular carcinoma (HCC) are hepatitis C virus, hepatitis B virus, and alcohol consumption, which can lead to cirrhosis, genomic instability, and progression to HCC. This process involves a cycle of regeneration and necrosis that induces release of cytokines, proangiogenic factors, and profibrotic factors. Fibrosis and increased cell proliferation can result in formation of a dysplastic nodule, marked genomic instability, loss of p53, and development of HCC [Farazi PA, DePinho RA. \u003Cem\u003ENat Rev Cancer\u003C\/em\u003E. 2006].\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EGastrointestinal Cancers\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EGastrointestinal Cancers\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EThe main risk factors for hepatocellular carcinoma (HCC) are hepatitis C virus, hepatitis B virus, and alcohol consumption, which can lead to cirrhosis, genomic instability, and progression to HCC. This process involves a cycle of regeneration and necrosis that induces release of cytokines, proangiogenic factors, and profibrotic factors. Fibrosis and increased cell proliferation can result in formation of a dysplastic nodule, marked genomic instability, loss of p53, and development of HCC [Farazi PA, DePinho RA. \u003Cem\u003ENat Rev Cancer\u003C\/em\u003E. 2006].\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ETARGETING MOLECULAR PATHWAYS IN HCC\u003C\/h2\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EJosep M. Llovet, MD, Mount Sinai School of Medicine, New York, New York, USA, discussed molecular pathways and targeted therapies for HCC. TERT promoter mutations are the earliest identified alterations in dysplastic liver nodules (25%) and the most frequent mutations in HCC (60%) [Nault JC et al. \u003Cem\u003ENat Commun\u003C\/em\u003E. 2013]. Other HCC mutations include CTNNB1 (24%), p53 (27%), Axin (8%), \u003Cem\u003ERAS\u003C\/em\u003E (\u223c 5%), PI3K (3%), ARID1a (12%), ARID1b (5.6%), and RPS6KA3 (9%) [Guichard C et al. \u003Cem\u003ENat Gen\u003C\/em\u003E. 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EThe most common high-level amplifications are 6p21 (vascular endothelial growth factor) and 11q13 (cyclin D1 and fibroblast growth factor 19 [FGF19]). Seven percent of patients have high amplification of vascular endothelial growth factor A [Chiang DY et al \u003Cem\u003ECancer Res\u003C\/em\u003E. 2008], which activates hepatocyte growth factor secretion [Horwitz E et al. \u003Cem\u003ECancer Discov\u003C\/em\u003E. 2014]. In a retrospective study, patients with this amplification had markedly improved survival when treated with sorafenib [Horwitz E et al. \u003Cem\u003ECancer Discov\u003C\/em\u003E. 2014]. High-level FGF19 and CCND1 amplifications occur in HCC; tumorigenicity of HCC cells with the 11q13 amplicon is inhibited by blocking FGF19 or CCND1 [Sawey ET et al. \u003Cem\u003ECancer Cell\u003C\/em\u003E. 2011].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EOther signaling pathways implicated in the development of HCC may provide potential targets for molecular therapies (\u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E).\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/14861\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/14861\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14861\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-6\u0022 class=\u0022first-child\u0022\u003ESignaling Pathways Implicated in the Development of HCC\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-8\u0022\u003ESorafenib\u2014an oral multikinase inhibitor of the vascular endothelial growth factor receptor, platelet-derived growth factor receptor, and Raf\u2014has been the standard of care for HCC since the 2008 pivotal SHARP trial [Llovet JM et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E. 2008]. Molecular therapies for HCC have been tested in \u0026gt; 300 Phase 2\/3 trials, 56 of which are ongoing. Among 2014 Phase 3 trials, 11 of 18 have been stopped or had inconclusive or negative results.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003ESeveral Phase 1 and 2 studies are testing novel therapies against specific targets in HCC. Tivantinib, a MET inhibitor, causes cell death with or without MET amplification, acting on microtubule dynamics independently of MET [Michieli P, Di Nicolantonio F. \u003Cem\u003ENat Rev Clin Oncol\u003C\/em\u003E. 2013]. A Phase 3 study is investigating tivantinib for second-line therapy in patients with MET-positive HCC [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01755767\u0026amp;atom=%2Fspmdc%2F14%2F22%2F24.atom\u0022\u003ENCT01755767\u003C\/a\u003E].\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ECHOOSING THE OPTIMAL TREATMENT FOR HCC\u003C\/h2\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EChris Verslype, MD, PhD, University Hospital Leuven, Leuven, Belgium, discussed HCC treatment options for patients on the liver transplant waiting list. The Sorafenib as Adjuvant Treatment in the Prevention of Recurrence of Hepatocellular Carcinoma trial [STORM; \u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT00692770\u0026amp;atom=%2Fspmdc%2F14%2F22%2F24.atom\u0022\u003ENCT00692770\u003C\/a\u003E] tested sorafenib versus placebo in patients with no residual disease following resection or ablation. The primary end point of relapse-free survival was not met, with median survival of 33.4 months in the sorafenib group versus 33.8 months in the placebo group (HR, 0.940; 95% CI, 0.780 to 1.134; p = .26; \u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Bruix J et al. \u003Cem\u003EJ Clin\u003C\/em\u003E Oncol. 2014 (suppl; abstr 4006)]. Sorafenib also did not improve overall survival (OS).\u003C\/p\u003E\n         \u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/22\/24\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Sorafenib Versus Placebo: Relapse-Free Survival\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-516801480\u0022 data-figure-caption=\u0022Sorafenib Versus Placebo: Relapse-Free Survival\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/22\/24\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/22\/24\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/22\/24\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14860\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-11\u0022 class=\u0022first-child\u0022\u003ESorafenib Versus Placebo: Relapse-Free Survival\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003ESource: Bruix J et al. \u003Cem\u003EJ Clin Oncol\u003C\/em\u003E 2014 (abstr 4006).\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EWithout therapy, patients with HCC on the transplant waiting list have a \u0026lt; 20% probability of dropping out at 6 months and \u0026lt; 40% at 12 months [Llovet JM et al. \u003Cem\u003EHepatology\u003C\/em\u003E. 1999]. There have been no randomized controlled trials of optimal bridging treatments for waiting list patients. The European Association for the Study of the Liver\u2014European Organisation for Research and Treatment of Cancer clinical practice guidelines recommend treatment with local ablation or chemoembolization when waiting times are estimated to exceed 6 months [Llovet J et al. \u003Cem\u003EJ Hepatol\u003C\/em\u003E. 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EThe evidence on radiofrequency ablation and transcatheter arterial chemoembolization (TACE) as bridging therapies is based on several studies. Survival after transplant is good in most radiofrequency ablation studies, but the intention-to-treat survival is more variable. The results of the TACE studies are also quite variable.\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EAfter bridging therapy, it is necessary to measure the response and monitor complications. Pretransplant imaging is correct in only 57% of patients, with understaging in 38% and overstaging in 5% [Galal A et al. \u003Cem\u003EHBP Dis Int\u003C\/em\u003E. 2013]. In patients with complete necrosis of the original tumor, 3-year OS and disease-free survival (DFS) are both 100%; for partial necrosis, OS is 78% and DFS is 75% [El-Gazzaz G et al. \u003Cem\u003EHepatobiliary Pancreat Dis Int\u003C\/em\u003E. 2013]. Vandecaveye et al [\u003Cem\u003ERadiology\u003C\/em\u003E. 2014] evaluated the relationship between response assessment and progressive-free survival (PFS) in patients treated with TACE. They found that the apparent diffusion coefficient ratio was a significant independent predictor of PFS (p \u0026lt; .001), with 93.3% accuracy.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EAccording to Prof Verslype, HCC recurrence following locoregional treatment is the rule, and sorafenib does not prevent this. Little is known about the most appropriate management of patients waiting for transplantation, despite the availability of many therapies. The success of bridging on intention-to-treat survival depends on the tumor biology and response to therapy. Current unmet needs for management of patients on the waiting list include tools to assess tumor biology and early assessment of a maintained response to therapy.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ENEW MOLECULAR TARGETED AGENTS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EAndrew X. Zhu, MD, PhD, Harvard Medical School, Boston, Massachusetts, USA, overviewed current treatments and new molecular targeted agents for HCC. Sorafenib is the only systemic agent approved for the treatment of HCC, but it has modest efficacy in advanced HCC with Child A cirrhosis. Although there are no validated biomarkers for sorafenib in HCC, a few potential biomarkers have emerged (\u003Ca id=\u0022xref-table-wrap-2-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T2\u0022\u003ETable 2\u003C\/a\u003E).\u003C\/p\u003E\n         \u003Cdiv id=\u0022T2\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/14862\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/14862\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14862\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 2.\u003C\/span\u003E \n               \u003Cp id=\u0022p-17\u0022 class=\u0022first-child\u0022\u003EPotential Biomarkers of Sorafenib Efficacy in HCC\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-19\u0022\u003ESeveral Phase 3 trials in advanced HCC have failed to demonstrate any benefit of treatment with sunitinib [Cheng AL et al. \u003Cem\u003EJ Clin Oncol\u003C\/em\u003E. 2013], brivanib [Johnson PJ et al. \u003Cem\u003EJ Clin Oncol.\u003C\/em\u003E 2013; Llovet JM et al. \u003Cem\u003EJ Clin Oncol\u003C\/em\u003E. 2013], linifanib [Cainap C et al. ASCO GI Symposium. 2012 (abstr)], erlotinib [Zhu A et al. ESMO 2012 (abstr)], or everolimus [Zhu A et al. \u003Cem\u003EJAMA\u003C\/em\u003E. 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-20\u0022\u003EA number of novel targeted therapies for HCC are currently undergoing testing in Phase 1 and 2 trials (\u003Ca id=\u0022xref-table-wrap-3-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T3\u0022\u003ETable 3\u003C\/a\u003E).\u003C\/p\u003E\n         \u003Cdiv id=\u0022T3\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/14863\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/14863\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/14863\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 3.\u003C\/span\u003E \n               \u003Cp id=\u0022p-21\u0022 class=\u0022first-child\u0022\u003ENovel Targeted Therapies for HCC\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-23\u0022\u003EThe presenters in this session reviewed the treatment strategies and approaches for the treatment of HCC that have been and are currently under investigation. Thus far, sorafenib is the only systemic agent approved for HCC. Dr Zhu concluded that other novel agents with unique mechanisms of action should be explored. Identifying predictive markers and applying molecular classification are important for predicting response and enriching the population in future HCC trials.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/22\/24.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzlztd\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzlztd\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzlztd\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}