Genistein in Soybeans May Halt Prostate Cancer Spread

Genistein, an antioxidant found in soybeans, almost completely prevented the spread of human prostate cancer in mice, according to a study published in the journal Cancer Research. In the study, genistein was used in an amount equivalent to what a human being would consume in a soybean-rich diet.

Genistein decreased metastasis of prostate cancer to the lungs by 96% compared with mice that did not eat the compound, the first demonstration that genistein can stop prostate cancer metastasis in a living organism. "These impressive results give us hope that genistein might show some effect in preventing the spread of prostate cancer in patients," said the study’s senior investigator, Raymond C. Bergan, MD, director of experimental therapeutics for the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

"Diet can affect cancer and it doesn’t do it by magic," Bergan said. "Certain chemicals have beneficial effects and now we have all the preclinical studies we need to suggest genistein might be a very promising chemopreventive drug."

Bergan has already shown in prostate cell cultures that genistein slows detachment of cancer cells from a primary prostate tumor, and checks cell invasion. It does this by blocking activation of p38 MAP kinases, molecules which regulate pathways that activate proteins that loosen cancer cells from their tight hold within a tumor, pushing them to migrate. "In culture, you can actually see that when genistein is introduced, cells flatten themselves in order to spread out and stick strongly to nearby cells," he said.

Researchers implanted groups of mice with an aggressive form of prostate cancer, having first fed them genistein. The amount of the chemical in the mouses’ blood was equivalent to human blood concentrations after eating soy foods, said Bergan. Genistein stopped lung mestasis almost completely, although it did not reduce the size of the tumors that developed within the prostate. Repeating the experiment produced he same result.

The size of tumor cells’ nuclei in the animals’ tissue was checked, to see whether he cells had flattened t in rder to spread. "Within a tumor, it is hard to tell where the borders of cells stop, so one way to measure adherence is to look at the size of the nuclei in cells and see if they are wider due to cell spread," Bergan said. "And that is what we found, demonstrating that the drug is having a primary effect on metastasis."

"What we think is happening here is that the cells we put in the mice normally like to move. When genistein restricted their ability to do so, they tried to compensate by producing more protein involved in migration. But genistein prevented those proteins from being activated," he said. "This is really a lesson for researchers who depend on biomarker studies to test whether a treatment is working. They need to be aware that those biomarkers might be telling only half of the story."

Source: Cancer Research, a journal of the American Association for Cancer Research. March 15, 2008.

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