Soy compound may prevent spread of prostate cancer

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Washington, Mar 14 : Researchers at the Northwestern University have revealed that a compound found in soybeans might help prevent the spread of prostate cancer.

In the study, conducted on mice, the researchers found that a chemical in soy - genistein - decreased metastasis of prostate cancer to the lungs by 96 percent compared with mice that did not eat the compound.

This is the first study to demonstrate 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.

In previous studies, Bergan and his colleagues have demonstrated in prostate cancer cell cultures that genistein inhibits detachment of cancer cells from a primary prostate tumour and represses 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 tumour, 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.

In the current study, the researchers fed genistein to several groups of mice before implanting them with an aggressive form of prostate cancer.

Bergan said that the amount of genistein in the blood of the animals was comparable to human blood concentrations after consumption of soy foods.

Following the study, Bergan and his research team found that while genistein didn't reduce the size of tumours that developed within the prostate, it stopped lung metastasis almost completely and they found the same result after repeating the experiment.

Then, the researchers examined tissue in the animals, measuring the size of tumour cells' nuclei to determine if the cells had flattened out in order to spread.

"Within a tumour, 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. And that is what we found, demonstrating that the drug is having a primary effect on metastasis," Bergan said.

Bergan said it was also found that mice fed genistein expressed higher levels of genes that are involved in cancer cell migration which, at first might not make sense in light of the study's conclusion that genistein almost completely blocked 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.

The study is published in the March 15 issue of Cancer Research, a journal of the American Association for Cancer Research.

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