Implications of the network structure of cellular control circuits for the design of anti-cancer vaccine therapies

I describe the use of a statistical mechanical model of a heirarchical network of failure-prone elements as a model for the failure of a network of interconnected biological elements that are or could be involved in the causation of cancer. From its topology, such a model predicts some of the properties of observed oncogene/tumour suppressor gene networks. I show that the same model suggests that a cancer vaccine strategy that targets ‘key’ network elements, such as p53 or RAS gene products, is not the only effective strategy for a broadly effective anti-cancer therapy. A mixed antigen or whole cell strategy could be as effective as single antigen vaccines, even if the latter are targeted at the most commonly mutated gene products.