Zachary Schug, Ph.D.

Zachary Schug, Ph.D.


The Schug Laboratory



Assistant Professor, Molecular & Cellular Oncogenesis Program

About the Scientist

Schug is interested in investigating metabolic adaptation in cancer cells through the use of cell biology, biochemistry, and metabolomics. 

After completing his B.S. in Biology from Saint Joseph’s University, Schug continued his studies in Philadelphia and earned a Ph.D. in Molecular Cell Biology from Thomas Jefferson University. In 2008 he began his post-doctoral studies at the Beatson Institute in Glasgow, United Kingdom and became a Research Assistant Professor during his time there. Zachary joined the Wistar Institute in 2016 as an Assistant Professor. Schug also holds an adjunct faculty position in the Department of Systems Pharmacology and Translational Therapeutics at the University of Pennsylvania.

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The Schug Laboratory

Alterations in the acquisition and metabolism of nutrients are now firmly recognized as hallmarks of cancer development. Many, if not all, oncogenes and tumor suppressor genes induce metabolic reprogramming in cancer cells through changes in the regulation of enzymes and transporters. These changes are necessary for cancer cells to meet the combined biomass and energy demands for growth and are only satisfied by increased capture and synthesis of cellular building blocks such as sugars, fats, and proteins. However, cancer cells often invade other tissues where the availability of certain nutrients is drastically different or grow so quickly that the blood supply, and the accessibility to oxygen and other nutrients that comes with it, becomes scarce. During these conditions of nutrient stress, many cancer cells will adapt and use other resources to survive.

The Schug laboratory is interested in identifying and therapeutically targeting the metabolic changes that arise during the development of cancer as well as in response to drug resistance. They combine cell biology, biochemistry, metabolomics, and genomics to uncover novel metabolic vulnerabilities in cancer. These targets are then fed into an active drug discovery program to develop effective therapeutic strategies for the improved treatment of cancer patients.


Postdoctoral Fellows

Jessica Casciano, Ph.D.
Katelyn Miller, Ph.D.

Research Assistant

Adam Cohen-Nowak

Selected Publications

Bulusu, V., Tumanov, S., Michalopoulou, E., van den Broek, N.J., MacKay, G., Nixon, C., Dhayade, S., Schug, Z.T., Vande Voorde, J., Blyth, K., Gottlieb, E., Vazquez, A., Kamphorst, J.J. "Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation." Cell Rep. 2017 Jan 17;18(3):647-658. doi: 10.1016/j.celrep.2016.12.055.

Schug, Z.T., Vande Voorde, J., Gottlieb, E. "The metabolic fate of acetate in cancer." Nat Rev Cancer. 2016 Nov;16(11):708-717. doi: 10.1038/nrc.2016.87. Epub 2016 Aug 26.

Peck, B., Schug, Z.T., Schulze, A., et al. "Inhibition of fatty acid desaturation is detrimental to cancer cell survival in metabolically compromised environments." Cancer Metab. 2016 Apr 1;4:6. doi: 10.1186/s40170-016-0146-8. eCollection 2016.

Patella, F., Schug, Z.T., Zanivan, S., et al. "Proteomics-based metabolic modeling reveals that fatty acid oxidation (FAO) controls endothelial cell (EC) permeability." Mol Cell Proteomics. 2015 Mar;14(3):621-34. doi: 10.1074/mcp.M114.045575. Epub 2015 Jan 8.

Schug, Z.T., Peck, B., Gottlieb, E., et al. "Acetyl-CoA synthetase 2 promotes acetate utilization and maintains cancer cell growth under metabolic stress." Cancer Cell. 2015 Jan 12;27(1):57-71. doi: 10.1016/j.ccell.2014.12.002.

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