Kurt Degenhardt, PhD
Assistant Professor, Department of Basic Biomedical Sciences
Dr. Degenhardt attended Kutztown University and earned a BS. in Biology. Following several years as a research technician he attended Stony Brook University/ Cold Spring Harbor Laboratory and earned a Ph.D. from the Department of Molecular and Cellular Biology. His dissertation is titled “Regulation of ras function by the guanine nucleotide exchange factor son-of-sevenless (Sos).” With his Ph.D., he joined Rutgers University as a Post-Doctoral fellow and was promoted to Assistant Research Professor. Following a short time as an Assistant Professor at St. John's University, he joined TouroCOM as an Associate Professor and Course Director of Physiology.
Education/Training
Ph.D. Biochemistry and Molecular Biology
Stony Brook University
Professional Affiliations
New York Academy of Sciences
Courses Taught
Physiology
Areas of Research
Cancer Biology- The roles of apoptosis and autophagy in tumor formation
Active cancer researcher on the fifth floor of TouroCOM Harlem
Grants/Funding
Determine altered gene expression patterns in response to metabolic stress-induced autophagy (2012). Touro Office of Sponsored Programs, Year 2 Faculty Research Grant Competition, Award: $4000
Invited Presentations
Doctoral Seminar: Department of Biology St. John's University (2010) Presented research entitled "The Role of Cell Death in Tumor Formation"
Hematology/Oncology Student Organization (2012)Presented research entitled “The role of cell death in tumor formation”
Research Department Fireside Chat (2012)Presented research entitled "Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis
Selected Publications
Degenhardt, K., and White, E. (2006).A mouse model system to genetically dissect the molecular mechanisms regulating tumorigenesis. Clin Cancer Res 12, 5298-5304.
Degenhardt, K., Mathew, R., Beaudoin, B., Bray, K., Anderson, D., Chen, G., Mukherjee, C., Shi, Y., Gelinas, C., Fan, Y., et al. (2006). Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. Cancer Cell 10, 51-64
Degenhardt, K., Sundararajan, R., Lindsten, T., Thompson, C., and White, E. (2002b). Bax and Bak independently promote cytochrome C release from mitochondria. J Biol Chem 277, 14127-14134.
Degenhardt, K., Chen, G., Lindsten, T., and White, E. (2002a). BAX and BAK mediate p53-independent suppression of tumorigenesis. Cancer Cell 2, 193-203
Kumar P, Zhang DM, Degenhardt K, Chen ZS. (2012) Autophagy and transporter-based multi-drug resistance.
Cells. 3, 558-75.