- PhD, 1979, University of Minnesota
- BS, 1975, Chemical Engineering, University of Illinois, Urbana-Champaign
The Lauffenburger laboratory emphasizes integration of experimental and mathematical/computational analysis approaches, toward development and validation of predictive models for physiologically-relevant behavior in terms of underlying molecular and molecular network properties. Our work has been recognized as providing contributions fostering the interface of bioengineering, quantitative cell biology, and systems biology. Our main focus has been on fundamental aspects of cell dysregulation, complemented by translational efforts in identifying and testing new therapeutic ideas. Applications addressed have chiefly resided in various types of cancer (including breast, colon, lung, and pancreatic cancers along with leukemias and lymphomas), inflammatory pathologies (such as endometriosis, Crohn's disease, colitis, rheumatoid arthritis, and Alzheimer's disease), and the immune system (mainly for vaccines against pathogens such as HIV, malaria, and tuberculosis). We have increasingly emphasized complex tissue contexts, including mouse models, human subjects, and tissue-engineered micro-physiological systems platforms in association with outstanding collaborators. From our laboratory have come more than 100 doctoral and postdoctoral trainees. Many hold faculty positions at academic institutions in the USA, Canada, and Europe; others have gone on to research positions in biotechnology and pharmaceutical companies; and others yet have moved into policy and government agency careers.
- American Association for the Advancement of Science, Member, 2019
- American Academy of Arts and Sciences, Fellow, 2001
- John Simon Guggenheim Memorial Foundation, Guggenheim Fellowship, 1989
- Oncogenic KRAS Regulates Tumor Cell Signaling via Stromal Reciprocation. Tape, CJ, Ling, S, Dimitriadi, M, McMahon, KM, Worboys, JD, Leong, HS, Norrie, IC, Miller, CJ, Poulogiannis, G, Lauffenburger, DA et al.. 2016. Cell 165, 1818.
- Reduced Proteolytic Shedding of Receptor Tyrosine Kinases Is a Post-Translational Mechanism of Kinase Inhibitor Resistance. Miller, MA, Oudin, MJ, Sullivan, RJ, Wang, SJ, Meyer, AS, Im, H, Frederick, DT, Tadros, J, Griffith, LG, Lee, H et al.. 2016. Cancer Discov 6, 382-99.
- CD4+ T cell-dependent and CD4+ T cell-independent cytokine-chemokine network changes in the immune responses of HIV-infected individuals. Arnold, KB, Szeto, GL, Alter, G, Irvine, DJ, Lauffenburger, DA. 2015. Sci Signal 8, ra104.
- The AXL Receptor is a Sensor of Ligand Spatial Heterogeneity. Meyer, AS, Zweemer, AJ, Lauffenburger, DA. 2015. Cell Syst 1, 25-36.
- Intratumor heterogeneity alters most effective drugs in designed combinations. Zhao, B, Hemann, MT, Lauffenburger, DA. 2014. Proc. Natl. Acad. Sci. U.S.A. 111, 10773-8.
Photo credit: Kathy Wittman