After completing his PhD in genetics at the Pennsylvania State University, Dr. Peffley did postdoctoral training in molecular biology at the University of Colorado School of Medicine in Denver, Colorado. His first faculty position was in the Department of Pharmacology at the University of Tennessee Health Sciences Center in Memphis, Tennessee. At this institution, Dr. Peffley obtained his first NIH grant that focused on cholesterol synthesis.
Dr. Peffley then moved to the Rosalind Franklin School of Medicine in North Chicago, Illinois where he was promoted to associate professor in the Department of Pharmacology and Molecular Biology. His research interests moved from cholesterol research to the dietary prevention of cancer. To support this research, Dr. Peffley received an NIH grant from the National Cancer Institute.
A promotion to full professor lead Dr. Peffley to the Kansas City University of Medicine and Bioscience in the Department of Pharmacology. At this institution he continued his research in dietary prevention of cancer as well as teaching pharmacology, genetics and biochemistry. While in Kansas City, Dr. Peffley finished his Juris Doctor in law at the University of Missouri Kansas City School of Law. He has also served as founding faculty at two medical schools including Edward Via College of Osteopathic Medicine and The University of South Carolina School of Medicine Greenville.
Dr. Peffley's research interests focus on dietary prevention of cancer by plant-derived terpenes or isoprenoids derived from the plant mevalonate biosynthetic pathway. Terpenes have potent antitumor effects and it is believed that diets rich in plant products provide some degree of protection from cancer (chemopreventives). Research has established that terpene-mediated antitumor actions are due in part to suppression of the mechanistic target of rapamycin (mTOR). mTOR is a serine/threonine kinase belonging to the family of phosphatidyl-3-kinase (PI3K) related kinases (PIKK). The mTOR activity is elevated in many tumor cells and has been associated with elevated translation of proteins required for cell cycle regulation and other metabolic processes. Suppression of the mTOR pathway in tumor cells leads to cell death through autophagy.