Fighting cancer is similar to the war against terrorism. Current cancer models suggest that a network of several cell mutations is needed to begin a cancer. Both terrorism and current models of cancer have complex origins that make it difficult to find simple causes or easy targets that can be tackled to solve either problem. Treatment of developed cancers also resembles the methods used to deal with established terrorist networks - aggressive therapies to destroy the cancer/terrorism with high risks of damage to healthy tissue/ non combatants.
But new work by Dr. Stella Pelengaris, and Dr Mike Khan at the University of Warwicks Molecular Medicine Research Centre has undermined the old complex model of how a cancer start and identified a single protein known as c-Myc as a mission-critical target for effective cancer therapies.
c-Myc is a protein which when switched on grows more cells when the body needs them. Sometimes it fails to switch off or switches itself on when it is not wanted. Normally our bodies have a fail safe mechanism which causes cells to commit suicide if c-Myc malfunctions in this way. This switching on of c-Myc and the failure of the cell suicide mechanism are two of the mutations required to start a cancer. However many researchers currently believe that many more mutations are also required if a cancer is to develop, for instance a mutation for developing a new blood supply required to nourish the growing cancer and mutation to allow cancerous cells to escape, travel the body and spread the cancer etc.
The researchers were not convinced by the need for a complex set of mutations and decided see what would
Contact: Dr. Mike Khan
University of Warwick