Cancer cachexia is a debilitating pathology of advanced cancer and increases mortality. Cancer cachexia reduces quality of life, limits chemotherapeutic options, and increases mortality. Maintaining muscle mass and function is dependent upon the balance between rates of protein synthesis and degradation, and changes in mitochondria function. The long-term goal of our research program is to improve skeletal muscle mass and function in cachexia. W are working to determine novel mechanisms that lead to skeletal muscle atrophy and weakness that occur across the spectrum of disease from prior to weight loss through severe muscle wasting. We are using a multifaceted approach to interrogate changes in muscle mass, muscle function, metabolism, and intracellular mitochondrial communication. We are using a novel therapeutic approach to improve muscle function in vivo. Understanding physiology in vivo using genetically modified mice has a strong history of improving patient care, and we are taking advantage of novel genetic tools to understand the full suite of REDD1 (regulated in development and DNA damage response 1) functions in skeletal muscle in response to cellular stress. We have generated a skeletal muscle-specific and inducible REDD1 KO mouse (msiREDD1-KO) and are using solid tumor metastasis to bone in these mice as a model system of cachexia and musculoskeletal impairment. We are investigating 1) balance between protein synthesis and degradation, and 2) regulation of mitochondrial metabolism, and 3) dysregulation of intracellular mitochondrial-SR tethering and communication.
Post-doctoral Fellowship - Indiana University School of Medicine, Indianapolis, IN 2006-2011
Ph.D. - Northwestern University, Evanston, IL 2004
