A pre-requisite for tumour growth and metastasis is angiogenesis, the sprouting and growth of new
capillaries from pre-existing blood vessels. Tumours without the ability to induce the growth of new capillaries
remain small, in the order of 1-2 mm3 [1]. Drugs are now available, such as Bevacizumab, to inhibit angiogenesis
and human tumour growth. Hepatocellular carcinoma (HCC) is a very aggressive human cancer, has clear
angiogenic characteristics and patients with HCC have a very poor clinical outlook. In this context, we review the
mechanisms of the predominant angiogenic pathways and how their targeting can impact on liver tumour growth.
We also discuss the role of hepatitis in influencing liver tumour blood vessel growth. Equally, the role of the
hepatic manifestation of the metabolic syndrome, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic
steatohepatitis (NASH) is considered, since it is now one of most common causes of liver disease in Western
Societies. There are links between angiogenesis and metabolism and although poorly researched in respect of
HCC, these we examine as they may impact on liver tumour formation and progression. Finally, we report on the
current status of trials of anti-angiogenic HCC therapy and consider the potential limitations of such a therapeutic
strategy.
Keywords: Angiogenesis, hepatocellular carcinoma, anti-angiogenic therapy.
