An experimental cancer drug that targets a common genetic fault has been shown to shrink tumours by up to 67 per cent in just six weeks.

Scientists tested their newly developed anti-cancer drug AMG 510 on four patients, two of whom saw their tumours shrink. It did not work for the others.

In studies on mice, the treatment helped to shrink, and in some cases eradicate, the growing tumours.

The daily pill works by turning 'off' the KRAS gene. Mutated forms of the genes are permanently trapped 'on', causing cancerous cells to multiply.

This abnormal activity fuels the development of up to 50 per cent of lung cancers, as well as some pancreatic and bowel cancers.

An experimental cancer drug that targets common genetic fault has been shown to shrink tumours by up to 67 per cent in just six weeks (pictured)

The pharmaceutical company described their findings as a 'milestone' for patients with cancer KRAS-mutant cancers.

The research was led by by pharmaceutical company Amgen Research, based in Thousand Oaks, California.

The findings, published in Nature, are the first to report the effects of inhibiting KRAS with a drug.

The KRAS gene provides instructions for making a protein called K-Ras that tells cells to grow and divide or mature and take on functions.

It belongs to a class of genes known as oncogenes. When mutated, oncogenes have the potential to cause normal cells to become cancerous.

AMG 510, an oral medication, stops the activity of this oncogene, Dr Jude Canon and his colleagues at Amgen revealed.

In mouse models of KRAS-mutant cancer, the treatment helped to shrink, and in 20 per cent of the cases, eradicated the growing tumour.

Then, in the first known clinical trial of a KRAS inhibiting drug, AM510 was given to four patients with non-small-cell lung carcinoma (NSCLC) who were not responding to treatment.

In two of the patients, improvements were seen in their tumour size. However, for the other two patients it did not work.

After six weeks of treatment, the patient who received a dose of 180mg saw their tumour shrink by 34 per cent. The second patient, who had 360mg, saw a reduction of 67 per cent.

What's more, in mice with bowel cancer, the treatment made the tumour more sensitive to other cancer drugs and generated a stronger immune response - an effect known as a pro-inflammatory microenvironment.

Taken together, the results suggest the drug could work well alone or in combination with other anti-cancer strategies.

KRAS has become an attractive drug target, however pharmaceutical development has been hindered because a binding site isn't clear.

The team found a surface groove called His95 in KRAS. AMG 510's potency is ten-fold higher when it latches on to the groove.

The drug is a 'breakthough', according to Professor Terence Rabbitts, from the MRC Weatherall Institute of Molecular Medicine, University of Oxford, who was not involved in the research.

He said: 'The protein KRAS is very often altered in cancer in many different ways and these changes are a major factor in cancer development.

'The KRAS protein had been thought to be undruggable, although it is not the first drug-like compounds to be described that binds to KRAS.

'It is important to understand that the drug will not be useful in all cancers and in fact only in those cancers where a very special change has occurred in KRAS.'

Professor Eric O'Neill, a professor of cell and molecule biology, University of Oxford, who was not involved in the study, also urged caution.

He said: 'The milestone is that this appears to have some clinical activity - the initial inhibitor was developed some time ago.

'Importantly this drug would not work in patients that do not have the specific KRAS mutation (Kras 12C).'

Lung cancers, of which around 85 per cent NSCLC, are very difficult to treat and for most people their cancer will return after treatment.

Survival is poor - around 35 per cent of patients will survive their cancer for five years or more after diagnosis despite being diagnosed early. The rates worsen the later the cancer is diagnosed.