David Potter
,
Credentials
MD, PhD

Professor of Medicine, Division of Hematology, Oncology and Transplantation
Faculty and Preceptor, Microbiology, Immunology and Cancer Biology (MICaB) Ph.D. Graduate Program
Preceptor, Medical Scientist Training Program (Combined MD/PhD Training Program)
Biography

Bio

Administrator Info
Name: Ms. J. Knapp
Phone: 612-626-1422
Fax: 612-625-6919
Email: jknapp@umn.edu
Mail: 420 Delaware Street SE, MMC 480, Minneapolis, MN 55455

Summary
After undergraduate studies in biology at M.I.T., Dr. Potter received M.D. and Ph.D. degrees from 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 in the laboratory of Dr. Phillip Sharp. 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 Breast Cancer Program at the Masonic Cancer Center.

Research Summary

  • Novel therapeutics for breast cancer

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 will be used to assay EET regio- and stereoisomers. These studies will promote further development of epoxygenases as targets for breast cancer therapeutics.

Clinical Summary

Novel therapeutics for breast cancer

Education

PhD, Johns Hopkins University
MD, Johns Hopkins University

Honors and Recognition

Outstanding Clinical Teacher, Inidian University School of Medicine
2004
Walther Prize for Cancer Research, Walther Cancer Institute
2004
Excellence in Teaching Award, Tufts University School of Medicine
1999
Phi Beta Kappa

Professional Memberships

Cancer Biology Training Grant Steering Committee, Breast ISC Team Leader
MSTP/MD, PhD Program Steering Committee, Translational Oncology Course Co-Leader
American Society for Biochemistry and Molecular Biology, Member
American Association for Cancer Research, Member
American Society of Clinical Oncology, Member