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Last Updated: Tuesday, 27 April, 2004, 10:28 GMT 11:28 UK
How some cancer cells cheat death
Two drugs may be better than one
Researchers have discovered how some cancer cells avoid being killed by chemotherapy.

Anti-cancer drugs trigger death in most cancer cells - but some cheat death by putting their growth on hold.

Cancer Research UK scientists found this process seems to be controlled by a protein molecule called p300.

The study, published in Procedings of the National Academy of Sciences, raises hope of boosting chemotherapy by blocking the protein.

We need new approaches to tackle difficult forms of the disease and targeting this molecule looks like a promising approach

Professor Robert Souhami
The discovery of the key role of the protein may also lead to new ways to predict which patients will respond to treatment.

Scientists knew p300 was involved in regulating a gene - called p53 - which protects cells from the effects of DNA damage that could lead to cancer.

If cells look like they may turn cancerous p53 suspends their growth or triggers their suicide mechanism.


Anti-cancer drugs, which work by damaging DNA, exploit this mechanism in cancer cells with an intact p53 gene.

When tumours are exposed to chemotherapy p53 is activated so that the cancer cell dies or stops growing.

But what determines whether the cancer cell is successfully killed off or just put to sleep has remained unclear until now.

Researcher Professor Carlos Caldas, based at the University of Cambridge, said: "It seems that cancer cells make a choice between life and death when attacked with chemotherapy.

"Finding out how this process is controlled will help us design ways to make anti-cancer drugs more effective in treating the stubborn forms of the disease."


The researchers compared the effect of UV radiation on human cancer cells that had p300 and those that were missing the molecule.

They found that cells with p300 only partially activated p53 and stopped growing but remained alive.

However, cells without p300 could fully activate p53 and trigger their suicide mechanism in response to DNA damage.

The team also tested the effect of a number of chemotherapy agents on cells with and without p300 and found the same effect - cells with p300 frequently failed to die whereas identical cells lacking p300 triggered their suicide machinery.

Professor Caldas said: "The molecule seems to safeguard cancer cells from the effects of chemotherapy.

"Designing drugs to target p300 and block its action could make current anti-cancer drugs more potent particularly against the resistant forms of the disease.

"We could also use the molecule as a way to predict whether tumours will be responsive to chemotherapy prior to treatment."

Professor Caldas is currently running a large study to determine if the combined analysis of p53 and p300 status in patients' tumours could be used to determine prognosis.

Professor Robert Souhami, Director of Clinical and External Affairs at Cancer Research UK, said: "We need new approaches to tackle difficult forms of the disease and targeting this molecule looks like a promising approach."

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