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.
Bains
W
W
Amedis Pharmaceuticals, Cambridge, UK. william.bains@amedis-pharma.com
D000951:Antigens, Neoplasm; D001699:Biometry; D019496:Cancer Vaccines; D015195:Drug Design; D006801:Humans; D019563:Mechanics; D018448:Models, Immunological; D009369:Neoplasms / Q000276:immunology / Q000628:therapy
D000951:Antigens, Neoplasm; D019496:Cancer Vaccines