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New Clues About Prostate Cancer

Mice without tumor suppressor gene develop condition similar to early stage disease

FRIDAY, Sept. 3, 2004 (HealthDayNews) -- Scientists have identified what may be the earliest step in the development of prostate cancer, the second leading cause of cancer death in American men.

The researchers bred mice lacking a single copy of a gene known to suppress tumors and found the animals developed a precancerous condition similar to the earliest stages of human prostate cancer.

The study appears in the Sept. 1 issue of Cancer Research.

"We've known for a long time that a class of genes called tumor suppressor genes are usually inactivated or somehow their function is lost in cancers, including prostate," said study author Norman Greenberg, a professor of clinical research at the Fred Hutchinson Cancer Research Center in Seattle.

His team focused on a tumor suppressor gene called the Rb gene, known to be defective in a variety of cancer types, including up to 60 percent of human prostate cancers. The Rb and other tumor suppressor genes normally work to keep cells dividing at a healthy pace.

Traditional thinking has it that there are usually two copies of these tumor suppressor genes in each healthy cell, Greenberg said, and you would need to lose both copies for a tumor to appear. But the study with mice proved otherwise, he said.

Using genetically engineered mice, the researchers were able to show that lacking just one copy of the Rb gene was enough to give the mice a condition akin to the earliest stages of human prostate cancer, Greenberg said.

"If they lost the second copy it was no more severe," he said of the cancer that followed. "But losing one copy was enough to get it going."

There are no immediate practical applications to the research, Greenberg said. But the hope is that eventually tests can be developed to distinguish between men who have only Rb mutations and those who have additional genetic defects associated with prostate cancer, such as the loss of the p53 tumor suppressor gene. That knowledge could help doctors decide when or whether aggressive treatment is needed, he said.

"We think this [loss of the single copy of the Rb gene] may be the earliest genetic lesion," Greenberg said. "It may in fact represent one of the earliest changes."

Based on what is known now, for instance, if a man had only an Rb lesion, "watchful waiting could be a good course," Greenberg said, referring to the decision not to perform treatment on prostate cancer because it appears to be slow growing.

Dr. Len Lichtenfeld, deputy chief medical officer for the American Cancer Society, said the new finding could prove promising. "It's fair to say they have honed in on a genetic change that appears to play a role. We have to emphasize that this experiment they did was in mice, not men."

Even so, Lichtenfeld said, the idea that the development of prostate cancer is a series of steps, not a single genetic malfunction, parallels what has been discovered about colorectal cancer. The new finding about prostate cancer "has to be taken forward and studied more, to see if we can develop a practical test to see if the change can be detected," he said.

But one of the treatment challenges, particularly for prostate cancer, is to determine which cancers will be aggressive and which won't, Lichtenfeld added. Focusing on the genetic changes might someday help doctors do that better, he said.

About 30,000 men are expected to die in the United States this year from prostate cancer, and another 230,000 will learn they have the disease. The prostate is a walnut-sized gland that sits below the bladder and supplies fluid for sperm during ejaculation.

More information

For more on prostate cancer, visit the American Cancer Society.

SOURCES: Norman Greenberg, Ph.D., professor, clinical research, Fred Hutchinson Cancer Research Center, Seattle; Len Lichtenfeld, M.D., deputy chief medical officer, American Cancer Society, Atlanta; Sept. 1, 2004, Cancer Research
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