Broccoli, Cauliflower May Help Suppress Hereditary Cancers

A new study shows that specific vegetables—cauliflower and broccoli, in particular--have natural compounds that may decrease the risk of developing hereditary cancers.

A research team from Rutgers, The State University of New Jersey (New Brunswick, NJ, USA), has revealed that these widely eaten cruciferous vegetables--so called because their four-petal flowers look like crosses--are abundant in sulforaphane (SFN). This compound had earlier been shown to suppress some tumors in rodents induced by carcinogens, compounds external to the body. This study, however, centered on whether SFN might suppress the occurrence of hereditary cancers--those originating from an individual's genetic structure.

The American Cancer Society estimates that more than two-thirds of cancer may be prevented through lifestyle adaptations, and nearly one-third of these cancer occurrences can be attributed to diet alone. "Our research has substantiated the connection between diet and cancer prevention, and it is now clear that the expression of cancer-related genes can be influenced by chemopreventive compounds in the things we eat,” said Dr. Ah-Ng Tony Kong, a professor of pharmaceutics in the Ernest Mario School of Pharmacy at Rutgers.

Chemopreventive properties are those that prevent, block, or reverse the development of cancer. In a study published online in May 2006 in the journal Carcinogenesis, Dr. Kong and his colleagues utilized a mouse model for human colon cancer to demonstrate the chemopreventive abilities of SFN and explained how it functions to inhibit cancer at the biomolecular level.

The investigators used a specially bred strain of mice (labeled Apc/Min/+) that carry a mutation that switches off a gene (Apc) that inhibits tumors. This is the same gene known to be involved in the development of most colon cancers in humans. When the gene is inactivated in the mice, polyps, which lead to tumors, appear spontaneously in the small intestine. Studies using these mice can help in devising human clinical trials that can lead to new treatments for colon cancer in humans.

Two groups of mice were fed diets supplemented with SFN for three weeks, one group receiving 300 parts per million (ppm) of SFN and the other getting 600 ppm. "Our results clearly demonstrated that those mice fed with an SFN-supplemented diet developed significantly fewer and smaller tumors,” Dr. Kong said.

After the three weeks, the median number of polyps in the small intestine in each mouse decreased more than 25% in those on the 300 ppm diet and 47% in the 600 ppm treatment group, as compared to control animals who had received no SFN.

"Our results showed that SFN produced its cancer preventive effects in the mice by inducing apoptosis [programmed cell death] and inhibiting proliferation of the tumors; however, it was not clear what mechanism SFN employs to accomplish this,” Dr. Kong stated.

Utilizing biomarkers (indicator molecules) associated with apoptosis and proliferation, the researchers discovered that SFN suppressed certain enzymes or kinases that are highly expressed both in the mice and in patients with colon cancer. The researchers concluded that this enzymatic suppression activity is in all probability the basis for the chemopreventive effects of SFN.

"Our study corroborates the notion that SFN has chemopreventive activity. Based on these findings, we feel SFN should be evaluated clinically for its chemopreventive potential in human patients with Apc-related colon cancers,” Kong said.



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