Broccoli, cauliflower and genetic cancer

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Public release date: 17-May-2006

http://www.eurekalert.org/pub_releases/2006-05/rtsu-bca051706.php

Contact: ph Blumberg

blumberg@...

x652

Rutgers, the State University of New Jersey

Broccoli, cauliflower and genetic cancer

Sulforaphane shown to inhibit the occurrence of hereditary colon cancer

NEW BRUNSWICK/PISCATAWAY, N.J. � Need another reason to eat vegetables?

A new study at Rutgers shows that certain vegetables � broccoli and

cauliflower, in particular � have natural ingredients that may reduce

the risk of developing hereditary cancers.

A research team led by Rutgers' Ah-Ng Tony Kong has revealed that these

widely consumed cruciferous vegetables � so called because their

four-petal flowers resemble crosses � are abundant in sulforaphane

(SFN). This compound had previously been shown to inhibit some cancers

in rodents induced by carcinogens � substances or agents external to the

body. Kong's investigations, however, focused on whether SFN might

inhibit the occurrence of hereditary cancers � those arising from one's

genetic makeup.

The American Cancer Society estimates that more than two-thirds of

cancer may be prevented through lifestyle modification, 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 Kong, a professor of pharmaceutics in the Ernest School

of Pharmacy at Rutgers, The State University of New Jersey.

Chemopreventive properties are those that prevent, stop or reverse the

development of cancer. In a study published online in the journal

Carcinogenesis, Kong and his colleagues used a mouse model for human

colon cancer to demonstrate the chemopreventive power of SFN and explain

how it works to thwart cancer at the biomolecular level.

The researchers employed a specially bred strain of mice (labeled

Apc/Min/+) that carry a mutation that switches off a gene (Apc) that

suppresses tumors. This is the same gene known to be directly implicated

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. Experiments using these mice can

help in designing 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, " Kong said.

After the three weeks, the average number of polyps in the small

intestine in each mouse decreased more than 25 percent in those on the

300 ppm diet and 47 percent 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, " Kong said.

Using biomarkers (indicator molecules) associated with apoptosis and

proliferation, Kong's team found 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 the likely 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.

--

ne Holden, MS, RD < fivestar@... >

" Ask the Parkinson Dietitian " http://www.parkinson.org/

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