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Beyond the Basics: The Differential Effects of Demographics and Hepatitis Status on Treatment Outcome in Hepatocellular Carcinoma

dothelial growth factor (VEGF)-A ligand and erlotinib, an oral tyrosine kinase inhibitor of the epithelial growth factor receptor. Of note, VEGF and epidermal growth factor pathways share a common downstream cascade of events and eventually stimulate angiogenesis signaling [4–6] . Additionally, upregulation of VEGF has been implicated in resistance to epithelial growth factor receptor inhibition [7] . Recent studies, including ours, indicated a signal of activity of both agents in HCC [8–12] . The authors report a progression-free survival at 16 weeks (PFS16) of 35.3% [95% confidence interval (CI) 22.4–49.9], a median PFS of 2.9 months (95% CI 1.3–4.42) and a median overall survival (OS) of 10.7 months (95% CI 6.2– 15.2) while grade 3/4 adverse events were not common. Results from our recent study [8] of the same combination in patients with advanced HCC in the US showed an overall higher magnitude of benefit with PFS-16 of 64% (95% CI 51–76), a median PFS of 7.2 months (95% CI 5.6–8.3) and a median OS of 13.7 months (95% CI 9.6– 19.7). Notably, there was a significant difference between the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections in both cohorts: 17 and 29% in our US cohort as compared to 82 and 8% in the Asian study, respectively [3] . Hepatocellular carcinoma (HCC) is the most common primary neoplasm of the liver, accounting for about 700,000 newly diagnosed patients per year, and more than two thirds of new HCC cases are from the Asia-Pacific (AP) region [1] , mainly linked to chronic hepatitis B infection. Although the incidence of HCC is particularly high in parts of Asia and sub-Saharan Africa, recent studies have reported a clear rise in the number of cases in Western Europe and the United States, largely because of the increase in hepatitis-C-related liver disease [2] . Unfortunately, most patients with HCC are not candidates for any curative treatments because of advanced disease at presentation and/or a background of advanced chronic liver disease. Furthermore, the growth of HCC depends on stimulatory effects of various growth factors, which bind to tyrosine kinase receptors and hence activate various intracellular signaling pathways which subsequently lead to tumor cell proliferation, survival, migration and metastasis. However, HCC is an angiogenesis-driven tumor, characterized by proangiogenic cytokine upregulation, hypervascularity and early vascular invasion. The current study [3] accompanying this editorial reports on an Asian cohort of 51 patients with advanced HCC who received the intravenous monoclonal antibody, bevacizumab, that binds to circulating vascular enPublished online: July 4, 2013