Scientists isolate faulty cancer gene that triggers the biggest breast tumours

The breakthrough could one day offer hope to millions of women by paving the way for better treatments for "basal-like breast cancer tumours".

These are the most dangerous and hardest to treat forms of the disease.

The research was welcomed by British cancer charities, but they stressed that new therapies were still many years away.

Scientists have known for more than a decade that mutations in a gene called BRCA1 put women at much higher risk of developing the aggressive "basal type" breast cancer.

These tumours grow fast, spread quickly and do not respond well to conventional drugs.

The risks are so high that some women with the BRCA1 mutations opt to have their breasts removed, rather than take a chance on getting cancer.

The BRCA1 mutations, inherited from parents, are carried by one woman in 800 and increase the risk by up to 85 per cent.

However, the reason why the BRCA1 gene is linked to cancer has been a mystery - until now.

Today, in a paper published in the science journal Nature Genetics, American experts have shown that

a faulty BRCA1 gene triggers cancer by disabling another vital gene, called PTEN.

PTEN, one of the body's "tumour suppressor" genes, wensures cells do not grow uncontrollably.

Normally the BRCA1 gene helps repair any mistakes that crop up in PTEN.

But if BRCA1 goes wrong, any faults in the PTEN gene remains unrepaired. Without its guiding hand, cells proliferate and form tumours.

"These findings are exciting because ever since the link was established between BRCA1 and breast cancer more than ten years ago, we have been frustrated by our lack of understanding about how mutations in this gene cause breast cancer," said Dr Ramon Parsons, of Columbia University, one of the paper's authors.

"We have been stymied by our limited resources to treat these cancers, which are associated with very poor prognoses.

"Now that we know that PTEN is involved, we finally have a target for therapy for these cancers."

A a fault in BRCA1 "is like cutting the brake cable on a car", he added.

"If PTEN is broken, you turn on a pathway that tells the cell to grow. It tells the cell to start dividing. It tells the cell, 'don't die'."

The team made the link by searching for faulty DNA in 34 biopsies from women with BRCA1 tumours.

The PTEN had been damaged and inadequately repaired in about two thirds of the cancers.

They estimate that around half of all BRCA1 cancers are started by unrepaired damaged to PTEN.

"A lot of drug companies are working on this. There is reasonably good hope that this approach will improve therapy for patients," Dr Parsons said.

Dr Lesley Walker, director of cancer information at Cancer Research UK, said the findings could lead to the development of new treatments.

"We urgently need to find new treatments for people with breast cancer who don't respond well to current treatments," she said.

"This is an important piece of science."