New test pinpoints deadliest prostate cancers

have found a new way to identify a particularly deadly form of prostate cancer in a breakthrough that could save tens of thousands of men from undergoing unnecessary surgery each year.

In contrast to many cancers, only certain prostate tumors require treatment. Many are slow-growing and pose little threat to health. But separating the "tigers" from the "pussycats" -- as oncologists dub them -- is tricky.

Now that is set to change with new research showing how a genetic variation within tumour cells can signal if a patient has a potentially fatal form of the disease.

"This will provide an extra degree of certainty as to whether a cancer is going to be aggressive or indolent, and that's really what we want to know," Colin Cooper, professor of molecular biology at Britain's Institute of Cancer Research, told Reuters.

"Many people get treated radically but probably two-thirds of them never needed treating," he added.

Radical prostate surgery often causes debilitating side effects such as impotence and incontinence, so any system that minimizes treatment would be a major boon to quality of life.

Cooper, who worked with Jack Cuzick at London's Wolfson Institute of Preventive Medicine on the new genetic marker, explained in a paper in the journal Oncogene how a particular genetic change could affect survival rates dramatically.
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Researchers knew that prostate cancers commonly contain a fusion of the TMPRSS2 and ERG genes, but the new study found that in 6.6 percent of cases this fusion was doubled up, creating a deadly alteration known as 2+Edel.

Patients with 2+Edel have only a 25 percent survival rate after eight years, compared with 90 percent for those with no alterations in this region of DNA.

"If you get two copies it's really bad news," Cooper said.

Exactly how the duplication makes tumours more aggressive is not clear, though Cooper speculates it could result in higher expression of proteins needed to drive tumour growth or be a more general indicator of genome instability.

Whatever the mechanism, 2+Edel is a clear-cut marker for risk that Cooper hopes will soon be used alongside existing techniques at the time of diagnosis to decide whether men require treatment.
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Currently, a system called the Gleason score is used to grade which cancers require treatment and which do not, but it is subject to variability in interpretation.
Doctors also use prostate specific antigen, or PSA, blood tests as a screen for early signs of prostate problems, though this test is not always a reliable indicator of cancer risk