Cell 'Addiction' to Growth Factors May Help Spur Cancers
THURSDAY Dec. 13, 2007 -- "Addiction" to certain growth factors contributes to the development of cancers caused by epigenetic changes, such as the inappropriate activation of a normally silent gene, scientists say.
The team of Johns Hopkins University researchers believe that blocking this addiction might help prevent cancer growth.
They compared mouse cells with only one copy of the IGF-II (insulin-like growth factor two) gene activated to mouse cells with both copies of IGF-II activated. Normally, only one copy of the IGF-II gene is activated.
In humans, activation of both IGF-II genes has been linked with a fivefold increased risk of intestinal tumors.
Mouse cells with one activated copy of the IGF-II gene responded to normal doses of IGF-II growth factor and recovered within 90 minutes. The cells with both copies of the IGF-II gene responded to the smallest doses of growth factor and stayed that way for more than 120 minutes.
Working with mice bred to develop colon cancer, the researchers then administered a drug that blocks the cell's ability to respond to IGF-II growth factor. The mice developed 70 percent fewer precancerous lesions than untreated mice.
"Finding the molecular mechanism behind cancer development allowed us to use a specific drug to actually take care of these risky cells before the animal developed cancer. It's making us think about cancer prevention in a whole new way," Dr. Andrew Feinberg, professor of medicine, oncology and molecular biology and genetics, and director of the Epigenetics Center at Hopkins, said in a prepared statement.
"If this is transferable to people, it could be really exciting," Feinberg said. "It means we might be able to do something about at-risk cells before cancer develops and treat these cells biochemically, and specifically, rather than using current drugs that are nonspecific and kill everything in their path."
The study was expected to be published online next week in the journal Proceedings of the National Academy of Sciences.
Posted: December 2007
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