The researchers, led by Bruce Boman, M.D., Ph.D., director of the Division of Genetic and Preventive Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia and at Jefferson's Kimmel Cancer Center and Dennis Leeper, Ph.D., professor of radiation oncology at Jefferson Medical College, say these results may have implications for treating patients with colon cancer, which is a tumor that frequently has mutations in a gene called APC.
They reported their findings this week at the 2006 annual meeting of the American Association for Cancer Research in Washington, D.C. (Stem Cell Number and Radiation Resistance During Repair in Colonic Crypts of APC Mice: Abstract no. LB-311).
Scientists have known that patients' colon tumors with APC mutations have an increased amount of survivin, a protein that halts the process of programmed cell death. This increase also appears to be associated with a rise in the number of stem cells that sit at the bottom of colonic crypts, tube-like structures that make up the lining of the intestine. Drs. Leeper and Boman wanted to see if there was a difference in stem cell number between normal mice and mice that carry a mutation in APC.
To do this, they exposed both normal and mutant mice to radiation, testing their ability to repair the resulting DNA damage. They speculated that increased survivin in the mutant mice might enable more stem cells to survive and affect the response to radiation. The researchers asked if mice with an APC mutation, making them prone to develop colon cancer, are different from normal mice in radiation s
Contact: Steve Benowitz
Thomas Jefferson University