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It's not all genetic: Common epigenetic problem doubles cancer risk in mice

k that the genetic mutation will cause a tumor," says postdoctoral fellow Atsushi Kaneda, Ph.D. "Double the risk may not seem like much, but this loss of imprinting is common."

The researchers' mice mirror two situations in people because the double dose of IGF2 was accomplished in two ways. One set of mice, obtained from Shirley Tilghman at Princeton, have a double dose of IGF2 because they are missing another gene, H19, whose sequence overlaps the region that usually shuts off one copy of IGF2. As a result, these mice lack H19 and have double IGF2.

To isolate the effect of the extra IGF2, Rolf Ohlsson at the Uppsala University, Sweden, developed a set of mice missing only the control region for IGF2; their H19 gene was intact. These mice likely mimic the 30 percent of colon cancer patients and 10 percent or so of the human population who have loss of imprinting of IGF2.

Only the Princeton mice have been crossed with the APC mice. Both the Princeton and the Swedish mice have the extra precursor cells in the lining of the colon, suggesting the effect on cancer development would be similar.

Co-author Dan Longo, M.D., of the National Institute on Aging notes that the mice with both double IGF2 and the APC mutation should be a useful animal model to evaluate the impact of colon cancer prevention strategies, including dietary interventions and targeted drugs.


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Source:Johns Hopkins Medical Institutions


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