They have identified a single protein known as c-Myc as a "mission-critical target for effective cancer therapies."

The scientists are from the University of Warwick's Molecular Medicine Research Centre and the University of California, San Francisco (UCSF).

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 Warwick and by Professor Gerard Evan of UCSF has undermined the old complex model of how a cancer starts 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.

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.

The Warwick and UCSF researchers were not convinced of the need for a complex set of mutations and decided to see what would happen if they introduced to pancreatic cells just the two mutations that would create the uncontrolled c-Myc.

Their experiments showed that they were correct and that within days a cancer was established just by switching on the c-Myc to build more unwanted cells and inhibiting the cell suicide fail-safe mechanism.

Dr. Pelengaris said, "People think cancer is very complicated, that you need half a dozen genetic lesions in order to get invasion. Our research provides a much more optimistic model. We've simplified it. We're saying that cancer isn't as complicated as people first thought. c-Myc may be one of several mission-critical targets for effective cancer therapies."

The researchers find several parallels between uncontrolled c-Myc and Bin Laden. This research makes c-Myc one of the biggest targets for those seeking to develop cancer therapies.

Just like Bin Laden, it is now a big target but not the only important cause (though elevated c-Myc levels are found in the majority of cancers). Lastly, as with Bin Laden, it is still best to catch and deal with the problem early before extensive support networks are developed.

This research finds that cancer can have simple non complex causes that give us more optimism in developing forms of treatment -- but if they are not detected early enough, cancers can still develop a complexity that is difficult to defeat.


[Contact: Dr. Mike Khan, Dr. Stella Pelengaris, Professor Gerard Evan]

16-May-2002