Hepatic resection and liver transplantation have been the mainstay curative treatments in HCC cases. The management of HCC has markedly improved since the early 2010s 8, 12, 13, 15. In terms of prevention, beyond vaccines preventing HBV infection and anti-viral therapies for HBV and HCV infection, cumulative data support the preventive role of coffee and aspirin 14. The diagnosis of HCC is usually based on non-invasive criteria, although there is a growing need for molecular characterization of the tumour using tissue biopsies in clinical practice 12, 13.
Currently, specific advancements in our understanding of the mechanisms underlying NASH-associated HCC have provided new insights into the contributions of the tumour microenvironment, particularly the immune system and platelet activation, in the pathophysiology of this disease 10, 11. In addition, the translation of molecular and immune classes into biomarkers that guide therapies is still under investigation.
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Indeed, dominant mutational drivers in HCC, such as TERT, TP53 and CTNNB1, remain undruggable 9. Approximately 25% of HCC tumours present actionable mutations however, the prevalence of most mutations is <10%, thereby complicating proof-of-concept studies 7, 8. Although our understanding of the pathophysiology and drivers of the disease has improved, this knowledge is yet to be translated into clinical practice. The molecular pathogenesis of HCC varies according to the distinct genotoxic insults and aetiologies. Additionally, reports on mutational signatures have established aristolochic acid and tobacco as potential pathogenetic cofactors in HCC 7. Non-alcoholic steatohepatitis (NASH), associated with metabolic syndrome or diabetes mellitus, is becoming the fastest growing aetiology of HCC, particularly in the West 6. Nonetheless, patients with cirrhosis are still considered to be at high risk for HCC incidence even after HCV clearance. The risk attributed to hepatitis C virus (HCV) infection has substantially decreased owing to patients achieving sustained virological response (SVR) with antiviral drugs 5. Hepatitis B virus (HBV) infection is the most prominent risk factor for HCC development, accounting for ~50% of cases 4. Hepatocellular carcinoma (HCC) is the most common form of liver cancer and accounts for ~90% of cases. It is estimated that, by 2025, >1 million individuals will be affected by liver cancer annually 3. Liver cancer remains a global health challenge and its incidence is growing worldwide 1, 2.
The outcomes of these trials are expected to change the landscape of HCC management at all evolutionary stages. New trials are exploring combination therapies, including checkpoint inhibitors and tyrosine kinase inhibitors or anti-VEGF therapies, or even combinations of two immunotherapy regimens.
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Six systemic therapies have been approved based on phase III trials (atezolizumab plus bevacizumab, sorafenib, lenvatinib, regorafenib, cabozantinib and ramucirumab) and three additional therapies have obtained accelerated FDA approval owing to evidence of efficacy. The current major advancements have impacted the management of patients with advanced HCC. Diagnosis based upon non-invasive criteria is currently challenged by the need for molecular information that requires tissue or liquid biopsies. Approximately 25% of all HCCs present with potentially actionable mutations, which are yet to be translated into the clinical practice. Moreover, non-alcoholic steatohepatitis-associated HCC has a unique molecular pathogenesis. Infection by hepatitis B virus and hepatitis C virus are the main risk factors for HCC development, although non-alcoholic steatohepatitis associated with metabolic syndrome or diabetes mellitus is becoming a more frequent risk factor in the West.
Liver cancer remains a global health challenge, with an estimated incidence of >1 million cases by 2025.
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