
Scientists have launched a pre-emptive attack on the development of resistance to cancer treatments.
They have discovered a genetic mechanism by which breast and ovarian cancer caused by a faulty BRCA2 gene could become resistant to treatment.
It is hoped the findings will both help doctors identify which patients might benefit most from treatment, and stop drugs from losing their effectiveness.
The study, by the Institute of Cancer Research, is in the journal Nature.
In 2004, over a quarter of a million people were diagnosed with cancer in the UK, and one in four deaths in the UK are caused by the disease.
By understanding this process we can alter patient treatment to counter the problem of resistance
Although diagnosis and treatment is improving, many tumours become resistant to treatment.
The faulty BRCA2 gene renders cells unable to repair damaged DNA, which can lead to them becoming cancerous.
Drugs, such as PARP inhibitors and the platinum-based chemotherapy drug, carboplatin, have been shown to be particularly effective against BRCA2 tumours in early laboratory trials.
They work by causing yet more DNA damage, tipping the cancer cells over the edge and killing them off.
More advanced trials of the drugs are currently underway in patients with BRCA2 breast and ovarian cancer - but there are concerns that some tumours would develop resistance.
The latest phase of the research on tumour cells in the laboratory showed that after exposure to the drugs, some cells are able to mutate back to the normal BRCA2 gene, allowing them to overcome DNA damage.
Unfortunately this does not neutralise the tumour - but potentially might neutralise the impact of the drugs.
The researchers found the same effect in tumour tissue taken from women with ovarian cancer.
Darwinism
Professor Alan Ashworth, director of the Breakthrough Breast Cancer Research Centre, said it was a clear example of Charles Darwin's natural selection theory - cancer cells are able to survive by changing the way treatments affect them.
"Drug resistance is a problem common to all types of cancer, yet this important process is poorly understood.
"Our work has shown how this occurs in some women with cancer. In the future we hope to be able to use this information to predict whether cancer patients will benefit from particular treatments."
"By understanding this process, we can alter patient treatment to counter the problem of resistance."
Professor Herbie Newell, Cancer Research UK's executive director of translational research, said: "This research deepens our understanding of why some breast cancer patients with a faulty BRCA2 gene may stop responding to treatment.
"This type of research is becoming increasingly important as we seek to tailor cancer therapies to individual patients."
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Latest News 28/08/08