Assistant Professor of Pharmacology & Cancer Biology
Jason W. Locasale, Ph.D. is a faculty member at Duke University in the School of Medicine. He graduated from Rutgers University, Summa Cum Laude with degrees in Chemistry and Physics. He received his Ph.D. at the Massachusetts Institute of Technology in Biological Engineering under the mentorship of Arup Chakraborty. He then conducted postdoctoral training Harvard Medical School under the guidance of Lewis Cantley as an American Cancer Society postdoctoral fellow and later as an Instructor on the faculty in the Department of Medicine.
Dr. Locasale has pioneered the use of metabolomics approaches to study cancer biology and metabolism. He has made seminal contributions to our understanding of metabolism including the role of serine synthesis in cancers, defining the quantitative, mechanistic principles of the Warburg Effect and altered glucose metabolism in cancer, and the role of metabolism in mediating chromatin status and epigenetics. His research combines quantitative approaches in metabolomics and mathematical modeling with biochemistry, cell biology and genetics.
Dr. Locasale is a recipient of the NIH Pathway to Indepence Award, the Benjamin Trump Award for Excellence in Cancer Research, and the American Cancer Society Research Scholar Award. Dr. Locasale currently serves on the editorial board of PLoS Biology and has numerous advisory roles for industry, the NIH common fund, and the National Cancer Institute. His laboratory is funded primarily by NIH. He has authored over 100 publications and numerous textbooks chapters and patents.
Quantitative approaches to understanding metabolism in cancer
Jason W Locasale Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham NC 27708
This presentation will discuss efforts to understand glucose and amino acid metabolism using metabolomics approaches. First I will discuss quantitative principles we are developing to target the Warburg Effect. The Warburg Effect is characterized by the increased metabolism of glucose and fermentation to lactate that occurs even in the presence of oxygen. Despite being a common feature of cancers and proliferative diseases, there are to date no major limitations in our understanding of its function and therapeutic strategies to interfere with it (while sparing normal glucose metabolism) are lacking. Next I will focus on a network known as one carbon metabolism that integrates nutritional status from multiple sources including glucose to generate multiple biological outputs including anabolic and redox metabolism. This network provides the substrates for methyl groups that mediate the epigenetic status of cells. I will discuss work on the variation in the basal activity of one carbon metabolism that is necessary and sufficient to determine methylation status of key epigenetic marks on histones and discuss data on dietary effects on the activity of the pathway. This finding provides a link between nutrient status and chromatin biology.
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