Xiaoyu Jiang1, John A. Engelbach2, Jeremy Cates3, Dinesh K. Thotala3, Robert E. Drzymala3, Dennis E. Hallahan3, Joseph JH Ackerman2, Joel R. Garbow2
1Chemistry, Washington University in St. louis, St. louis, MO, United States; 2Radiology, Washington University in St. louis, St. louis, MO, United States; 3Radiation Oncology, Washington University in St. louis, St. louis, MO, United States
Radiation necrosis is a severe, but late occurring, injury to normal tissue, within and surrounding a radiation treatment field. Increases in vascular permeability (leakiness) and acute vascular apoptosis have both been suggested as possible causes of radiation necrosis. Bevacizumab may help to repair leaky capillaries and thereby mitigate radiation necrosis. Specific inhibitors of GSK-3β, a serine/threonine kinase, are known to ameliorate apoptosis. We have recently developed a novel mouse model of radiation necrosis using Gamma Knife irradiation. Here, we use small-animal MRI to measure the mitigation of radiation necrosis by bevacizumab and SB415286, an inhibitor of GSK-3β, in this mouse model.