Analysing a tumor's genes can predict which prostate cancers won't need additional treatment and which cases require more intensive therapies.
Watchful waiting is a common strategy for treating prostate cancer, since in about 40 per cent of cases the tumors are so slow-growing that they don't require additional, invasive biopsies or treatment and men with the cancer are more likely to die of other causes.
But based on analyses of tissue from men whose prostates were surgically removed as a precaution even if they were deemed to be low-risk, anywhere from 15 per cent to 20 per cent of these low-risk cases actually turn out to involve tumors that were more aggressive.
As a result, the tumors were mischaracterised by available predictive methods such as the blood-based prostate specific antigen (PSA) test and imaging to search for hidden growths.
So researchers at Genomic Health, the company that developed a gene-based test for predicting which breast cancers might recur, turned their attention to creating a similar assay for prostate cancer.
The breast cancer assay, Oncotype Dx, provides women with a number between zero and 100 that indicates their risk of recurrence and their response to chemotherapy.
The prostate cancer panel, known as Oncotype Dx Genomic Prostate Score, is now available following release of the study results. Dr Peter Carroll, director of the department of urology at the University of California, San Francisco, led the independent trial that validated the new test.
"We wanted to see if we could improve the issue of risk assessment for prostate cancer patients," said Carroll.
Working with biopsy samples from 400 patients who had prostate surgery and were determined to be at low risk of recurring tumors, Carroll and his team found that the panel of 17 genes in the assay could reliably predict how aggressive the cancers were.
In some cases, the more active the genes were, the higher the risk of recurrence, while in others, less activity conferred the greater risk. When the researchers matched the activity of these genes to the men's prostate cancer outcomes, they were encouraged to see that in about half of the participants, the genetic assay proved to be an effective predictor of the tumor's aggressiveness; the genetic information moved the men's risk score (determined by the existing PSA and imaging tests) for developing additional tumors higher or lower by about five points.
For about 23 per cent of the men, the panel of genes changed the scores by ten points of more. "You might say that for most patients, the test provides them with some information," said Campell. "We think the information is significant in about half of patients and very significant in about a quarter."
The test included not just the panel of 17 cancer-related genes but an additional five control genes to ensure that researchers accurately measured when the genes were more or less active.
The 17 genes appear to be involved in cell growth, androgen hormone metabolism (which influences prostate function) and other tumor-related processes.
Carroll and his team presented the results on the test at the annual meeting of the American Urological Association.
Carroll is already planning a follow-up trial that will track 1,000 men prior to prostate cancer treatment to see if the genetic panel can accurately predict which men went on to develop aggressive disease and which ones did not–and which men might avoid treatments altogether.
The information could be helpful in providing more confidence in physicians'–and patients'–decisions to avoid treatments because men aren't likely to need them.
A genetic test that could determine men at the highest risk of developing aggressive disease could change how prostate cancer was treated, Carroll said, since doctors would be able to more accurately predict which men would need more rigorous follow-up and which men likely won't have to worry about their prostate that much. (Time.com)
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