Key find could prevent deadly prostate cancer

 

A blood test that can distinguish between the benign and dangerous forms of prostate cancer could soon be developed following a breakthrough in understanding the complex genetics behind the most common type of cancer in men.

Scientists believe they have identified a key difference between a "metastatic" prostate tumour that spreads to other parts of the body and a slow-growing tumour that does not. The finding could lead to a test for dangerous metastatic prostate cancer as well as new drugs that could prevent such tumours from spreading.

About 250,000 men in Britain live with prostate cancer but only a tiny fraction of these tumours will turn metastatic, which usually leads to death. One man in Britain dies of prostate cancer every hour, whereas 100 men per day will have the disease diagnosed.

Being able to distinguish between relatively benign, slow-growing tumours and aggressive cancers that are more likely to spread to other organs is one of the research priorities of cancer-funding organisations. Now a research team at the Cold Spring Harbor Laboratory in New York believes it may have found a vital clue that could lead to such a test.

"The ideal scenario is to be able to detect what we are looking for by taking blood samples, although that may prove to be too late. It might be better to pick up metastatic tumours by taking small biopsies from the prostate gland," said Professor Lloyd Trotman, who led the research team.

The study, published in the journal Cancer Cell, describes the relationship between three genes that all play a role in determining whether a prostate cell becomes cancerous and whether the resulting tumour is likely to spread.

The scientists found that a gene called PHLPP1 works in concert with another gene known as PTEN, which is mutated in about half of all prostate cancer sufferers. Normally both genes act as "tumour suppressors", which mean they prevent cancers from developing, but when they are both mutated, the result can lead to cancer.

A third gene, known a p53, also acts as a tumour suppressor and works like a "water sprinkler" when the two other genes are damaged to prevent the cancer "fire" from spreading further. However, when p53 is also mutated, a metastatic cancer is likely to develop, Professor Trotman said.

"This discovery led us to ask whether there are specific rules for prostate cancers to become lethal," he said. "In terms of diagnostic tests, having lost the three genes is a hallmark feature of many metastatic cancers. We could envisage a test that looks at the activity levels of these genes and whether they are en route to metastatic disease," he added.

It also opens the way to using drugs known to influence the metabolic pathways of these genes, which would have the effect of overriding damaged genes that would normally suppress tumours, Professor Trotman said.

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