MINNEAPOLIS / ST. PAUL--The substance that gives ginger its flavor appears to inhibit the growth of human colorectal cancer cells, according to research at the University of Minnesota's Hormel Institute in Austin, Minn. Working with mice that lack an immune system, research associate professor Ann Bode and her colleagues found slower rates of cancer growth in mice given thrice-weekly feedings of [6]-gingerol--the main active component of ginger. Bode and co-author Zigang Dong, director of the institute, will discuss the work at a press conference from 9:30 to 10:30 a.m. MST Tuesday, Oct. 28, during a meeting of the American Association for Cancer Research in the J.W. Marriott Desert Resort and Spa in Phoenix. They will also present the work at a poster session from 1 to 2:30 p.m. and from 6 to 7:30 p.m. MST in the Marriott.
"Plants of the ginger family have been credited with therapeutic and preventive powers and have been reported to have anti-cancer activity," said Bode. "The substance called [6]-gingerol is the main active compound in ginger root and the one that gives ginger its distinctive flavor."
The researchers tested [6]-gingerol's powers by feeding a half milligram to 20 mice three times a week before and after injecting human colorectal tumor cells into their flanks. Control mice were treated the same, except their food contained no [6]-gingerol. Tumors were allowed to grow until they reached a size of one cubic centimeter (0.06 cubic inch), after which the mice were euthanized. The mice, known as athymic nude mice, are often used in such studies because they provide a living-body environment in which tumors can grow without interference from an immune system.
The first tumors appeared 15 days after the cells were injected. At that time, 13 tumors of measurable size had appeared among the control mice, four among the [6]-gingerol-treated mice. Mice consuming [6]-gingerol lagged in both the number of animals with measurable tumors
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Contact: Deane Morrison
morri029@umn.edu
612-624-2346
University of Minnesota
28-Oct-2003
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