Research Program: Women's Cancer
Associate Professor, Department of Medicine

dapotter@umn.edu
612-625-8933 — office
612-626-7207 — lab
Preferred method of contact: e-mail

Dr. Potter's clinical profile
(University of Minnesota Physicians Web site)

David A. Potter, M.D., Ph.D., is an associate professor in the Department of Medicine. After undergraduate studies in biology at M.I.T., he received the M.D. and Ph.D. degrees from the Johns Hopkins University. He trained in internal medicine at Stanford University Medical Center, and in hematology and oncology at Tufts-New England Medical Center. He performed post-doctoral studies at the M.I.T. Center for Cancer Research. He was on the faculty at Tufts University, the Indiana University Cancer Center, and moved to the University of Minnesota in 2006, where he is a member of the Women's Cancer Research Program at the Masonic Cancer Center.

Dr. Potter's research interests include: the roles of calpain proteases in cancer, the roles of heat shock protein 90 in breast cancer, and translational breast cancer clinical trials.

Research Interests

Regulation of calpain proteases and their roles in cytoskeletal remodeling; the roles of cytochrome P450 in breast cancer progression.

Three enzymatic pathways of arachidonic acid metabolism, involving cyclooxygenases, lipoxygenases and epoxygenases, have been identified in mammalian cells, but only the first two have been mechanistically linked to human cancer. The HIV protease inhibitor ritonavir is a potent inhibitor of epoxygenases that arrests the growth of breast cancer xenografts, but its mechanism of action is unknown. Epoxygenases promote the production of epoxyeicosatrienoic acids (EET's) that activate Akt kinase. Our studies seek to determine whether epoxygenases are cancer therapeutic targets. The hypothesis to be tested is that epoxygenase activation promotes breast cancer progression by promoting Akt phosphorylation and cancer cell survival. Based on our observations we are asking the following questions: What are the molecular mechanisms by which epoxygenases cause growth dysregulation in breast cancer? Do epoxygenases enhance the transforming activities of oncogenes in mammary carcinoma? Do epoxygenase pathways require Hsp90 activity for cancer cell survival? Targeted lipidomics methods are being used to assay EET regio- and stereoisomers. These studies will promote further development of epoxygenases as targets for breast cancer therapeutics.

Selected Publications

Potter, D. A., J. S. Tirnauer, R. Janssen, D. E. Croall, C. N. Hughes, K. A. Fiacco, J.W. Mier, M. Maki  and I. M. Herman. 1998. Calpain regulates the actin cytoskeleton during cell spreading. J. Cell Biol. 141:647-662.

Croce, K., R. Flaumenhaft, M. Rivers, B. C. Furie, B. Furie, I. M. Herman and D. A. Potter. 1999. Calpain regulates platelet secretion, aggregation and spreading. J. Biol. Chem. 274:36321-36327.

Carragher, N.O., M.A. Westhoff, D. Riley, D. A. Potter, P. Dutt, J.S. Elce, P. A. Greer and M. C. Frame. 2002. v-src Induced Modulation of the Calpain-Calpastatin Proteolytic System Regulates Both Morphological Transformation and Cell Cycle Progression. Mol. Cell. Biol. 22:257-69.

D. A. Potter, Anjaiah Srirangam, K. A. Fiacco, D. Brocks, M. Maki , D. Acheson and I. M. Herman. 2003  Calpain Regulates Enterocyte Brush Border Actin Assembly and Pathogenic E. coli-Mediated Effacement. J. Biol. Chem. 278 (32):30403-30412.

Glading, A., R Bodnar, IJ Reynolds, H Shiraha, L Satish, DA Potter, HC Blair, A Wells. 2004. EGF activates m-calpain (calpain 2), at least in part, by ERK-mediated phosphorylation. Mol. Cell. Biol., 24 (6):2499-2512

Narayanasamy, D., S. Mukhopadhyay, M. Palakal and D. A. Potter. 2004. TransMiner: Mining Transitive Associations among Biological Objects from Text. Journal of Biomedical Science. 11 (6):864-873.

Henley, J. D., D. J. Summerlin, D. A. Potter, R. D. Timmerman and C. E. Tomich. 2005. Intraoral Mucin-Rich Salivary Duct Carcinoma. Histopathology 47(4):436-437.

Zhang, B., A. Srirangam, D. A. Potter and A. Roman. 2005. HPV16 E5 Protein Disrupts the c-Cbl-EGFR Interaction and EGFR Ubiquitination in Human Foreskin Keratinocytes. Oncogene. 24(15):2585-8.

Srirangam, A., R. Mitra, M. Wang, J. C. Gorski, S. Badve, L. A. Baldridge, J. Hamilton, H. Kishimoto, J. Hawes, L. Li, J. S. Blum, D. B. Donner, G. W. Sledge , H. Nakshatri and D. A. Potter. 2006. Effects of HIV Protease Inhibitor Ritonavir on Akt-Regulated Cell Proliferation in Breast Cancer. Clin. Cancer Res. 12: 1883-1896.

Carpenter, J. S., Rawl, S. R., Porter, J., Schmidt, K., Tornatta, J., Ojewole, F., Helft, P., Potter, D. A., Sweeney, C., & Giesler, R. B. 2008 Oncology outpatient and provider responses to a computerized symptom assessment system. Oncology Nursing Forum (in press)