Genetic Markers Predict Which Prostate Tumors Will Kill

A strand of double-stranded DNA, in the shape of a double helix.
A strand of double-stranded DNA, in the shape of a double helix. (Image credit: James. J. Caras, National Science Foundation)

A new study associates five genetic markers with fatal cases of prostate cancer.

During the 6.5-year study of prostate cancer patients, those who had four or all five of these genetic markers were 50 percent more likely to die from the cancer than those who had none, one or two of the markers, according to the researchers.

The findings may lead to the development of a blood test that could help distinguish between men who need aggressive cancer treatment and those that don't.

The genetic markers could be used in addition to risk factors already known to increase the risk of death from prostate cancer, such as the stage of cancer at the time of diagnosis, said study researcher Janet Stanford, co-director of the Prostate Cancer Research Program at the Fred Hutchinson Cancer Research Center in Seattle.

Together, these could "improve the clinical management of the disease by helping stratify which patients need the most aggressive approach to therapy and follow-up, as opposed to those at lower risk for having a fatal outcome from their disease," Stanford said.

Additional research would be needed to validate the markers in large populations.


About 200,000 men in the United States are diagnosed with prostate cancer every year, many through use of the PSA blood test. About one quarter to one third of these cancers are aggressive at the time of diagnosis and may require treatment such as surgical removal of the prostate.

But a large portion will be indolent — slow-growing cancers that don't cause significant health problems during the patient's lifetime, Stanford said. Currently, there is no good way to distinguish between the two groups. As a result, many patients with indolent cancer may be overtreated, Stanford said.

Stanford and colleagues analyzed blood samples from more than 1,300 prostate cancer patients, ages 35 to 74, in the Seattle area. They scanned 156 genes, looking for differences in the genome that were associated with lethal prostate cancer. They identified 22 such differences.

The researchers further analyzed those 22 markers in a separate group of about 2,800 prostate cancer patients in Sweden. They were able to associate five markers with lethal prostate cancer.

These markers are found within a patient's normal cells, not prostate cancer cells. The findings suggest men with prostate cancer who have these markers are predisposed to having the aggressive type, Stanford said. Some of these markers are in genes that control tissue growth, inflammation, blood-vessel development and bone density.

Predicting aggressive cancer

Scott Tomlins, a pathologist at the University of Michigan Medical School who was not involved in the study, said it's not clear whether identifying these markers will improve upon the information already used to predict prostate cancer's aggressiveness.

Only about 10 percent of men with prostate cancer in the study had all five markers, Tomlins noted. It's not certain whether identifying men in the general population who have these markers would improve our overall ability to predict aggressive disease, Tomlins said.

Future research should incorporate these markers into a model to see whether they improve predictions, but ultimately, we should study a number of factors to augment predictions, including genes of the prostate cancer itself, Tomlins said.

Pass it on: Five genetic markers may help predict which men with prostate cancer will have a more aggressive course of disease.

This story was provided by MyHealthNewsDaily, a sister site to LiveScience. Follow MyHealthNewsDaily staff writer Rachael Rettner on Twitter @RachaelRettner. Like us on Facebook.

Rachael Rettner

Rachael is a Live Science contributor, and was a former channel editor and senior writer for Live Science between 2010 and 2022. She has a master's degree in journalism from New York University's Science, Health and Environmental Reporting Program. She also holds a B.S. in molecular biology and an M.S. in biology from the University of California, San Diego. Her work has appeared in Scienceline, The Washington Post and Scientific American.