Health: Cell discovery leads to drugs rethink

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The Independent Online
Scientists are claiming that a discovery about the way cancer cells grow could lead to kinder treatments that are also more effective. Jeremy Laurance reports on a surprise finding.

Stopping cancers growing may be simpler than has been thought. Researchers have found that the signalling mechanism which determines whether a cancer cell lives or dies is located on its surface, not inside it protected by an impermeable membrane, and should therefore be an easier target for new drugs.

Scientists from the Imperial Cancer Research Fund say the discovery, published in the US journal Science, opens the way for a new generation of cancer drugs that would be less toxic than those currently used. Instead of poisoning the cancer cells, the new drugs would manipulate the appropriate on/off switches on their surface. This should mean an easier and safer way of treating patients with cancer.

Professor Gerard Evan, head of the research team, said: "The results have been totally unexpected. There was no reason to believe that the "abort" programme that destroys tumour cells should operate via the cell surface."

The growth of cells is known to be controlled by a process known as apoptosis, or cell suicide, which prevents any rogue cells taking over the body. In cancer, the suicide programme becomes blocked, leading to uncontrolled growth of the cells, resulting in a tumour.

Professor Evan said: "We have now found that the suicide programme is routed out of the cell and then back in through its surface. This new discovery of how cell death is triggered is very important for understanding how cancer cells arise. It also suggests novel ways of selectively attacking cancer cells without damaging normal ones."

Commenting on the finding, Andrew Wylie, professor of experimental pathology at the University of Edinburgh, said: "This new discovery will mean that drug companies can start to research a new generation of cancer drugs that may well increase survival rates."

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