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Tuesday, 13 March, 2001, 00:32 GMT
Common heart drug 'blocks cancer'
Blood cells
Drug blocks cancer cells ability to travel in the blood
Researchers have discovered how a drug commonly used to thin the blood also acts to block the spread of cancer.

They say the breakthrough should lead to trials on patients with newly diagnosed cancer as soon as possible.

It has been known for some time that the anticoagulant drug heparin can reduce the development of secondary cancer tumours.

But scientists have not known why the drug has this effect, and research in the area has failed to produce significant results.

Now a team from the University of California at San Diego has discovered the drug disrupts a crucial interaction between blood cells and cells from the initial site of the cancer.

This interaction enables the cancer cells to enter the bloodstream, so they can circulate around the body and establish potentially deadly secondary tumours elsewhere.

Researchers 'mistaken'

The research was carried out on mice
Lead researcher Dr Lubor Borsig said the previous research had mistakenly assumed that the anti-cancer effect of heparin was due to its ability to prevent blood clotting.

When cancer cells break away from the original tumour and enter the bloodstream they attract blood cells called platelets.

The platelets form a cloak around the cancer cells, which protects them from the body's immune system defences.

Heparin appears to disrupt the formation of this cloak - leaving the cancer cells exposed to attack by the white blood cells of the immune system.

The UCSD researchers gave mice a single dose of heparin, which lasted for only a few hours.

Yet even this limited exposure to the drug resulted in markedly reduced cancer cell survival and development of secondary tumours when the mice were examined several weeks later.

Professor Ian Hart, of the Imperial Cancer Research Fund said: "This research establishes a mechanism by which heparin works and shows that it doesn't only have an anticoagulant effect.

"However, the application of this knowledge to the clinical setting carries with it significant practical problems.

"Firstly, as it is difficult to predict the precise point at which a tumour will spread in humans, it would be necessary to keep patients on anticoagulant therapy for a long period, and this may have clinical implications.

"Secondly, there have been many large clinical trials of anticoagulant therapy in the past, which haven't shown great benefit for treating cancer, so knowing the mechanism by which heparin works may not make any difference."

The research is published in the Proceedings of the National Academy of Sciences.

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