Page last updated at 00:12 GMT, Saturday, 21 January 2006

Killer breast cancer therapy hope

Woman has a breast scan
Breast cancer is the most common form of the disease in the UK

Researchers have pinpointed the chemistry behind the development of a particularly aggressive form of breast cancer.

The Dana-Farber Cancer Institute team hope the discovery could lead to new, more effective drugs.

The complex chain of molecular interactions they have uncovered occurs in about 10% of breast cancers - including the deadliest ones.

The research appears in the journal Cancer Cell.

We are going to see in the next five years a movement away from treating all tumours with the same drugs
Dr Peter Sicinski

The first step in the chain that leads to breast cancer is the over-production of a common protein called cyclin D1 which helps to control cell growth.

This in turn over-stimulates a molecular switch, CDK4 kinase, causing it to unleash a virulent proliferation of cancer cells.

If these cells also contain a mutated cancer-causing form of a gene called HER2 they are notoriously difficult to treat.

In one recent study, the seven-year survival rate for women with this subgroup of breast cancers was only about 13%.

Drug combination

However, the drug Herceptin, currently the subject of much controversy as it is not yet widely available on the NHS, has shown some potential in blocking the HER2 mutation.

And other currently available anti-cancer drugs such as Gleevec work by blocking the action of kinases.

The Dana-Farber team believe it should be possible to develop a drug that specifically blocks CDK4, and then to use it in combination with Herceptin to treat patients with these particularly aggressive tumours.

Researcher Dr Peter Sicinski said: "We are going to see in the next five years a movement away from treating all tumours with the same drugs, and instead match specific drugs to tumours based on their molecular characteristics."

The researchers created laboratory mice with different combinations of genes to tease out the key chemistry.

They showed that not only was the cyclin D1 - CDK4 interaction responsible for creating cancer cells, it was also required for the cancer to continue to grow.

A separate study published in the same journal found mice with a form of cyclin D1 which could not activate CDK4 were not only developmentally normal, but highly resistant to HER2 breast cancers.

More work needed

Dr Sicinski said it would be difficult to design a drug to inhibit the action of cyclin D1, but blocking a kinase should be significantly easier.

Henry Scowcroft, of Cancer Research UK, said: "These results are exciting.

"They highlight the huge importance of studying the basic biology of cancer cells.

"Scientists now need to show that inhibiting CDK4 function can actually disrupt breast cancer growth, and then find a safe, reliable way of doing so in cancer patients who have been identified as suitable for this sort of therapy.

"This process may take many years. But results like these show the progress we are making in our understanding of how cancer develops, and how we could treat it even more successfully."

Dr Sarah Rawlings, of the charity Breakthrough Breast Cancer, said: "It is encouraging that research such as this is finding new ways of targeting aggressive breast cancers but this research is at a very early stage of development and it will be some time before treatments are available to breast cancer patients."

Dr Rawlings said women should regularly check their breasts, and consult a doctor if they discovered any change in shape and texture.

Clara MacKay, of the charity Breast Cancer Care the research could help the drive towards more personalised treatments - but agreed it was still at an early stage.

"Further work is needed to determine whether blocking the pathway that has been identified could be effective in treating particularly aggressive forms of breast cancer."



SEE ALSO
Stem cell may drive breast cancer
05 Jan 06 |  Health
'Speed up' cancer drug assessment
29 Dec 05 |  Health
Breast cancer
10 Jul 09 |  Health

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