Tammy Chilton Lee, M.S


Clinical Study Coordinator
Wake Forest School of Medicine



M.S., Molecular Medicine and Translational Science Graduate Program, August 2009
Wake Forest University School of Arts and Sciences

Biology concentration, Salem College, 2006 

BS, Business Administration and Economics, High Point University, 1984

Current Research:

An estimated 170,000 new cases of brain metastases occur each year in approximately 10 to 30% of adult cancer patients. Primary malignant central nervous system (CNS) tumors represent about 2% of all cancers, with more than 40,000 cases annually in the United States. Most of these patients will receive radiation therapy (RT), which can lead to injury to the normal brain. The symptoms of radiation-induced brain injury are described as acute, sub-acute, and chronic depending on the time of occurrence which can be hours, days, weeks and even years after radiation. The chronic phase, occurring approximately 6 months or more after radiation, is highly associated with progressive cognitive impairment. Radiation-related brain injury involves multiple cells and tissue types with varying biological changes

Currently, there are no effective treatments for radiation-induced brain injury. Selecting the correct time for intervention and reducing side effects associated with brain radiotherapy are critical. Our lab, under the leadership of Dr. Mike Robbins, investigates experimental strategies to determine and mitigate: i] activation of pro-inflammatory transcription factors, ii] upregulation of pro-inflammatory mediators and iii] expression of the brain renin-angiotensin system (RAS). I am conducting in vivo studies in rat models to test the hypothesis that inhibiting the intrinsic brain RAS using RAS blockers targeted at either angiotensin converting enzyme (ACE)1 or Ang II Type 1 receptors (AT1R) will ameliorate the development and progression of radiation-induced brain injury. Additionally, using well-defined in vitro models of normal brain cells, I will test the hypothesis that irradiation activates the intrinsic brain RAS, leading to a chronic and persistent oxidative stress/inflammatory response.

Given the complexities of radiation-induced changes, improved understanding of these processes and interactions will provide a mechanistic basis for optimization of treatment to improve the side effects and quality of life of long-term survivors of brain irradiation.



Lee, Tammy; Chilton, Floyd; Wilson, Martha; Willard, Stephanie; Shively, Carol: Marked Differences in Lipid Metabolism between Depressed and Nondepressed Monkeys: 2nd Annual Symposium: The Role of Dietary Fatty Acids in the Prevention and Treatment of Disease, October 2007


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Contact Information
Molecular Medicine and Translational Science Graduate Program

Office 336-713-4259

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