Hepatocellular carcinoma (HCC) is characteristically hypervascular, and therefore many antiangiogenic therapies are under clinical investigation. However, their therapeutic efficacies are still limited. While inhibition of angiogenesis results in tumor hypoxia and cell death, this may also activate a variety of hypoxia-induced cell growth and survival signals, which may promote HCC progression. Therefore, the simultaneous blockage of these signals may be essential in maximizing the efficiency of antiangiogenic therapies. Information regarding some of our experimental agents targeting these HCC signals is presented in this manuscript.

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