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Nutrition Health Review, Spring, 1993
In numerous population studies, diets high in fruits and vegetables has been associated with reduced risk of certain cancers. Research by John S. Bertram, Ph.D., of the Cancer Research Center at the University of Hawaii (Manoa), suggests that carotenoids (a group of natural pigments found in most fruits and vegetables) may prevent precancerous cells from growing uncontrollably into malignant tumors.
According to Dr. Bertram's hypothesis, cells begin to proliferate uncontrollably when they are cut off from signals from neighboring normal cells that regulate their rate of growth. "Carotenoids enhance communication between premalignant cells and normal cells, to help them behave more like normal cells," said Bertram.
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Dr. Bertram believes that enabling premalignant cells to receive growth-regulating signals from normal cells may suppress tumor growth. His work suggests a chemoprotective mechanism that is independent of beta carotene's role as a physiological antioxidant (compounds that help prevent damage to cells and tissues from highly reactive molecules known as free radicals).
Normally, signals that regulate growth and function of cells pass from one cell to the next through microscopic conduits in cell membranes known as gap junctions. Gap junctions are made of connexins (a specialized group of proteins) that align to form a channel from one cell to the next.
During the development of many cancers, a defect in the functioning of connexin proteins interferes with transmittal of cell-to-cell messages. It is believed that cells that have been cut off from the communication loop multiply unchecked because messages that regulate rate of proliferation are not being received.
"Premalignant cells become 'deaf' to these signals," explained Bertram. "Carotenoids 'switch on' the gene that codes for connexin proteins thereby increasing the number of properly functioning connexin proteins. This, in turn, forms more gap junctions, which enables cells to communicate more effectively," he added.
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