David Potter, MD, PhD

David Potter

420 Delaware ST SE
MMC 480
Minneapolis, MN 55455
United States

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.


Awards & Recognition

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


Professional Associations

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


Medical School, Johns Hopkins University, Baltimore, MD

Residency, Stanford University Medical Center, Stanford, CA

PhD, Johns Hopkins University, Baltimore, MD

Postdoctoral Fellow, M.I.T. Center for Cancer Research


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Research Summary/Interests

  • 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.

Research Funding Grants

Role: Principal Invetigator, Breast Cancer Research Program Grant, Department of Defense CDMRP

Grant Title: Potentiation of immune checkpoint blockade by inhibition of epoxyeicosatrienoic acid driven tumor respiration 



Breast Center

Board Certifications

  • American Board of Internal Medicine - Hematology
  • American Board of Internal Medicine - Oncology



Clinical Interests

Novel therapeutics for breast cancer