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Genetic trigger for prostate cancer 'found'
Researchers believe that they have discovered the genetic trigger for the most common male cancer and say the advance could revolutionise the way that the disease is diagnosed and treated.

Every year more than 30,000 men in Britain are diagnosed with prostate cancer and 10,000 die from it.

The discovery that the disease is caused by chromosomes scrambling and triggering abnormal cell growth could lead to a much more accurate diagnostic test in blood or urine than is provided by current screening.

The new find will help scientists to work out the best course of action for each type of prostate cancer and could pave the way to more effective treatments. It is also suspected that a similar mechanism could be at work in other common cancers, such as lung cancer.

Genes fuse together as a result of the scrambled chromosomes to produce abnormal gene activity, according to a study published yesterday in the journal Science by researchers at the University of Michigan Medical School, in collaboration with Brigham and Women's Hospital at Harvard.

The abnormal gene fusion occurs when one of two genes, ERG or ETV1, merges with a prostate-specific gene called TMPRSS2, team members Scott Tomlins and Daniel Rhodes discovered.

They found the unique molecular signature of these fused genes in around 75 per cent of prostate cancer tissue samples, but found no evidence of gene fusion in benign prostate tissue or in prostate tissue with non-cancerous changes.

"The data in our study provides evidence that gene fusion is the causative agent in prostate cancer," said Prof Arul Chinnaiyan, who directed the study. "It is the first step in the progression of tissue changes leading to prostate cancer.

It will allow us to categorise prostate tumours by molecular sub-type, which could help determine the most effective treatment for each patient."

While re-arrangements in chromosomes and fused genes have been detected in blood cell cancers such as leukaemia and lymphoma, this is the first time they have been found in a common solid tumour like prostate cancer.

The team hopes to identify small molecule inhibitors for the genes involved in prostate cancer, which would be similar to Gleevec, a drug designed to target the gene fusion that causes a form of leukaemia.

Prof Colin Cooper, a prostate cancer expert at Cancer Research UK, said: "This work is potentially very important in terms of understanding how prostate cancer develops, but the results must now be confirmed in a larger number of prostate cancer samples."

By Roger Highfield, Science Editor

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