The knowledge and understanding of all aspects of liver cancer [this including hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA)] have experienced a major improvement in the last decades. New laboratory technologies have identified several molecular abnormalities that, at the very end, should provide an accurate stratification and optimal treatment of patients diagnosed with liver cancer. The seminal discovery of the TP53 hotspot mutation [1,2] was an initial landmark step for the future classification and treatment decision using conventional clinical criteria blended with molecular data. At the same time, the development of ultrasound, computed tomography (CT) and magnetic resonance (MR) has been instrumental for earlier diagnosis, accurate staging and treatment advances. Several treatment options with proven survival benefit if properly applied are now available. Major highlights include: i) acceptance of liver transplantation for HCC if within the Milan criteria , ii) recognition of ablation as a potentially curative option [4,5], iii) proof of benefit of chemoembolization (TACE),  and iv) incorporation of sorafenib as an effective systemic therapy . These options are part of the widely endorsed BCLC staging and treatment model (Fig. 1) [8,9]. This is clinically useful and it will certainly keep evolving to accommodate new scientific evidence. This review summarises the data which are the basis for the current recommendations for clinical practice, while simultaneously exposes the areas where more research is needed to fulfil the still unmet needs (Table 1).
Bibliographical noteFunding Information:
JB is supported by a grant of the Instituto de Salud Carlos III (PI11/01830 and PI14/00962). CIBERehd is funded by Instituto de Salud Carlos III.
GJG is supported by grant DK59427 from the National Institutes of Health, and the Mayo Clinic.
VM is partially supported by grants of the Italian Association for Cancer Research (AIRC), the Ministry of Health: finalized cancer research and the National Transplant Centre (CNT).
J ML is supported by grants from The European Commission Framework Programme 7 (HEPTROMIC, Proposal No:259744), the Samuel Waxman Cancer Research Foundation, the Spanish National Health Institute (SAF2013-41027), and the Asociación Española Contra el Cáncer (AECC).
J Bruix has received research support from Bayer HealthCare Pharmaceuticals and consulting fees from Bayer HealthCare Pharmaceuticals, Onyx Pharmaceuticals, Arqule, Bristol-Myers-Squibb, BTG, Imclone-Lilly, Novartis, Terumo, Roche, Kowa and BioAlliance. GJ Gores has received consultancy fees from Bayer HealthCare Pharmaceuticals, Bristol-Myers Squibb, Chugai, Daiichi Sanyo, Delcath, Genentech, and Generon. Josep M. Llovet has received research support from Bayer Healthcare Pharmaceuticals, Bristol Myers Squibb and Boehringer-Ingelheim, abd consutancy fees from Bayer Healthcare Pharmaceuticals, Bristol Myers Squibb, Boehringer-Ingelheim, Lilly Pharmaceuticals, Celsion, Biocompatibles, Novartis, GlaxoSmithKline and Blueprint Medicines. V Mazzaferro declares conflict of interest due to consultancy with Bayer and BTG Biocompatibles having received consulting fees from the two. KH Han has received consulting fees from Eisai Pharmaceuticals and KOWA.
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