Eugene C. Butcher, M.D.

  • Director, Co-founder and Chair, SAB, LEUVAS Therapeutics
  • Klaus Bensch Professor in Pathology, Stanford School of Medicine

Eugene received a B.S. in Chemistry from the Massachusetts Institute of Technology and an M.D. from the Washington University School of Medicine, St. Louis, MO. In 1976, he began his residency training in Anatomic Pathology in the Dept. of Pathology at Stanford University.  After his clinical training and a postdoctoral fellowship with Dr. Irving Weissman, in 1982 he joined the Department of Pathology where he currently holds the Klaus Bensch Professorship. 

 Dr. Butcher's academic work has focused on the cellular and molecular mechanisms of lymphocyte and leukocyte trafficking in immunity and inflammation, and on systems level insights into mechanisms of cell-cell recognition and function.   He has made seminal contributions to our understanding of leukocyte trafficking and lymphocyte homing and their patho-physiological significance.   Butcher was the first to propose that multi-step adhesion cascades confer both specificity and diversity to tissue-tropic lymphocyte migration and he demonstrated how homing receptors, vascular addressins and chemokines, many of which were discovered in his laboratory, contribute to such multi-step adhesion cascades in secondary lymphoid organs, skin and gut. He demonstrated therapeutic inhibition of lymphocyte homing in animal models of inflammatory diseases, enabling targeted approaches to autoimmune and inflammatory diseases.   In particular, his molecular identification and functional characterization of the mucosal vascular addressin MAdCAM-1 and its lymphocyte receptor a4b not only revolutionized our understanding of mucosal immunology, but also led directly to the development of transformational treatments for inflammatory bowel diseases, including Vedolizumab which Butcher helped develop,  Pfizer's clinical stage anti-MAdCAM1 drug PF-00547,659, and Genentech’s Etrolizumab in trials for drug resistant IBD, the latter an antibody originally produced in the Butcher lab. 

Butcher’s work has received worldwide recognition and has earned a number of prestigious professional honors. He has been elected to the Association of American Physicians, and has been awarded the Warner Lambert/Parke Davis Award by the American Association of Pathologists, the Middleton Award, the AAI-Huang Foundation Meritorious Career Award by the American Association of Immunologists, and an Outstanding Inventor Award from Stanford University. He received the Crafoord Prize from the Swedish Academy of Sciences in 2004 for the scientific discovery of mechanisms of leukocyte trafficking, including elucidation of the multistep control of leukocyte recruitment, contributing to the treatment of inflammatory diseases. Dr. Butcher has also pioneered quantitative cell systems biology for chemical genomics and drug discovery, spearheading a new approach to human disease biology as a discovery science.  He is the author of over 300 peer-reviewed scientific articles and an inventor on nine US patents. He was Scientific Co-Founder and Co-Chair of the Scientific Advisory Board of Leukosite, Inc. (where he initiated development of Vedaluzimab) and has served on the Scientific Advisory Boards of Millennium, Medimmune, and other biopharmaceutical companies. He also co-founded and served as Director and Chair of the Scientific Advisory Board of Bioseek, Inc.

Selected Publications

1.  Gallatin, W. M., Weissman, I. L. & Butcher, E. C. A cell-surface molecule involved in organ-specific homing of lymphocytes. Nature 304, 30-34, (1983).
            The first identification of a homing receptor for endothelial cell recognition. 

2.  Streeter, P. R., Lakey-Berg, E., Rouse, B. T. N., Bargatze, R. F. & Butcher, E. C. A tissue-specific endothelial cell molecule involved in lymphocyte homing. Nature 331, 41-46, (1988).
          MAdCAM1, the first identified vascular addressin.  Anti-MAdCAM1 antibody specifically inhibited lymphocyte homing to the intestines and gut associated lymphoid tissues.

3.  Kishimoto, T. K., M. A. Jutila, E. L. Berg and E. C. Butcher (1989). Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors. Science 245(4923): 1238-1241.
            Rapid downregulation of L-selectin and upregulation of b2 integrins during neutrophil activation in vitro  or arrest on endothelium in vivo, indicating sequential engagement for leukocyte recruitment.

4.  Berlin, C. et al. a4b7 integrin mediates lymphocyte binding to the mucosal vascular addressin MAdCAM-1. Cell 74, 185-195, (1993).
         Defined Alpha 4 beta 7 as the integrin lymphocyte receptor for MAdCAM1. 

5.  Campbell, J. J. et al. Chemokines and the arrest of lymphocytes rolling under flow conditions. Science 279, 381-384, (1998).
        Showed that newly-discovered members of the chemokine family could differentially trigger the arrest of lymphocyte subsets under flowing conditions, confirming Butcher's predictions made in his 1991 Cell minireview.