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Hepatocellular carcinoma (HCC) is the second cause of cancer-related death and it represents the leading cause of death in patients with cirrhosis.1 The vast majority of HCCs develop in a background of severe liver fibrosis, commonly caused by HBV or HCV infection, exposure to aflatoxin B, alcoholic and non-alcoholic steatohepatitis (NASH), as well as genetic diseases.1 Despite recent advances in the treatment of viral hepatitis, modelling of the dramatic rise in the incidence of NASH predicts a substantial increase in the global burden of HCC.1
HCC allocation to treatment options is based on tumour number, size and vascular invasion, as well as on the functional liver reserve. Although HCC aggressiveness can be inferred from these clinical parameters, screening programmes in patients at risk increasingly detect early-stage HCCs that share homogeneous clinical features, but that diverge in terms of biological and molecular features.1 Therefore, a more precise prediction of HCC aggressiveness is expected from a better insight on HCC heterogeneity.
Liver transplantation is the most effective curative option for HCC though it suffers from obvious limitations such as donor (organ) shortage. Alternative treatments include hepatic resection and tumour ablation, chemoembolisation and systemic therapy, which is limited to sorafenib and lenvatinib as first-line treatment, and second-line options like regorafenib among others.1 Sorafenib, a multikinase inhibitor with antiproliferative and antiangiogenic properties, is the gold-standard systemic treatment option improving patient survival.1 Still, some tumours are resistant to sorafenib, underlining the urge to understand how HCC cells develop treatment resistance.
Cancer progression results from the coevolution of a heterogeneous ecosystem …
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