Major breakthrough in fight against the deadliest cancers

Scientists find way to shut off gene that causes third of all tumours Find could lead to drugs for most difficult to treat cancers More pancreatic, bowel and lung cancers could be cured New treatment would have fewer unpleasant side effects

The ' Everest' of cancer genes has been conquered by scientists. They have found a way of shutting off a gene that causes a third of all tumours, including some of the most deadly.

Despite advances in medicine, cancer kills more than 150,000 Britons a year - the equivalent of a life every four minutes.

The breakthrough could lead to new drugs for hard- to- treat cancers. As well as saving lives, the new treatments should have fewer side- effects than existing medicines.

The excitement surrounds a gene called ras, which when mutated can trigger the development of tumours, fuel their growth and keep them alive.

A drug that shuts it down has eluded some of the best brains in science for more than 30 years, leading many to believe it was unbeatable.

Now, US scientists have succeeded in making a chemical that kills ras- driven human lung cancer cells.

Researcher Kevan Shokat, of the Howard Hughes Medical Institute at the University of California, described the rogue gene as ' the Everest of cancer mutations'.

He said: ' People have tried to drug every part of ras and looked at every nook and cranny on it and screened a million compounds and never found anything that inhibits it well.

'We are very excited. We believe this has real implications for patients.' Cancers caused by the ras gene are particularly fast growing and spreading and difficult to treat.

' They include many pancreatic, lung and bowel cancers, which between them kill almost 60,000 Britons a year.

It is hoped that by shutting off ras, the new drug will stop the growth of tumours and shrink them.

Crucially, it acts only on the cancer- causing form of the ras gene, meaning healthy cells are spared. This should cut the risk of side-effects such as sickness, nausea and hair loss normally seen with cancer drugs.

Dr. Shokat, who has formed a company to commercialise his work, said: ' What is very special about this drug is that it only works in cells that have this particular mutation. That distinguishes it from every other cancer drug we know of.'

Dr. Frank McCormick, leader of a £ 6.2million US government initiative to tackle the ras gene, said: ' Cancers driven by ras are the most difficult to treat. Dr. Shokat and his team have taken a brilliantly innovative approach and have developed a strategy for targeting a mutant form of ras with exquisite specificity.'

The new drug works against one rogue form of ras but Dr. Shokat believes it should be possible also to make drugs that work against the other forms.

His chemical has so far been tested only on cells in a dish but a new medicine could be tested on people in three years and on the market by 2021. However, it will have to be shown to be safe and effective in large- scale trials on patients.

Dr. Emma Smith, senior science information officer at Cancer Research UK, said: ' This lab study is another step forward in finding ways to shut down an important molecule called ras, which is a key player in cancer development.

' And this molecule has been notoriously difficult to block with drugs.

' Ras is one of the most important molecules in cancer and when it goes wrong it can cause aggressive cancers that are hard to treat, so finding chemicals that stop it working is a vital area of research that could lead to potent new drugs in the future.'