'Wonder drug' to kill off cancer

'Wonder drug' to kill off cancer

An international team, led by University of California, says that the KG5 drug works by making cancer cells "commit suicide"; it stops tumorous cells multiplying and they then shut themselves down, the 'Nature Medicine' journal reported.

The radical drug will bring fresh hope to patients with aggressive and deadly tumours and could be available in as little as five years, say the scientists, who hope to deliver the it in pill form, which has very few side-effects.

Lead scientist Prof David Cheresh said the drug "blocks the function of proliferation" and the malignant cells commit suicide when they can't multiply. Proved effective in tests against pancreatic, breast and kidney cancers, it could well have a positive effect on a broad range of other tumours.

KG5 works in a totally different way to traditional therapies by altering the structure of a cancer growth protein, an enzyme known as RAF.

The protein has been long-studied, but its role in cell division -- critical to cell proliferation and tumour growth -- is a surprise. Existing treatments block RAF's activity. However, KG5 changes the entire shape of the protein, which neutralises it without leading to unwanted side-effects.

To date, KG5 has been tested in animals and tissue samples taken from patients.

The team has since developed variants of KG5 that are 100-fold more powerful than the original drug. They hope one of these more powerful compounds will enter clinical trials on humans at Moores Cancer Center in San Diego within 18 months.

"Before this drug was designed, we had no idea RAF could promote tumour cell cycle progression. This may be only one example of how, by designing drugs that avoid the active site of an enzyme, we can identify new and unexpected ways to disrupt the growth of tumours.

"In essence, we are attacking an important enzyme in a whole new way and thereby discovering new things this enzyme was intended for," the 'Daily Express' quoted Prof Cheresh.

At present, medicines that target enzymes like RAF often damage healthy cells, according to Prof Cheresh. "They hit many different targets, meaning they can produce undesired side-effects and induce dose-limiting toxicity," he said.

Rather than homing in on a particular part of the protein, the new class of RAF inhibitor alters the enzyme's whole structure. It singles out RAF in proliferating cells, while ignoring normal or resting cells. KG5 also acts by cutting off the blood supply to tumours.

Dr Julie Sharp of Cancer Research UK, welcomed the new findings, saying, "The next step will be to test out these ideas with patients."