Douglas Lauffenburger

Douglas Lauffenburger

Ford Professor of Biological Engineering, Chemical Engineering, and Biology; Head, Department of Biological Engineering

Douglas Lauffenburger fosters the interface of bioengineering, quantitative cell biology, and systems biology to determine fundamental aspects of cell dysregulation — identifying and testing new therapeutic ideas.

617-252-1629

Phone

16-343

Office

Gerri Powers

Assistant

617-253-7420

Assistant Phone

Education

PhD 1979, University of Minnesota

Research Summary

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.

Awards

  • American Academy of Arts and Sciences, Fellow, 2001
  • John Simon Guggenheim Memorial Foundation, Guggenheim Fellowship, 1989

Key Publications

  1. 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.
    doi: 10.1016/j.cell.2016.05.079PMID:27315484
  2. 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.
    doi: 10.1158/2159-8290.CD-15-0933PMID:26984351
  3. 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.
    doi: 10.1126/scisignal.aab0808PMID:26486173
  4. The AXL Receptor is a Sensor of Ligand Spatial Heterogeneity. Meyer, AS, Zweemer, AJ, Lauffenburger, DA. 2015. Cell Syst 1, 25-36.
    doi: 10.1016/j.cels.2015.06.002PMID:26236777
  5. 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.
    doi: 10.1073/pnas.1323934111PMID:25002493

Recent Publications

  1. Route of immunization defines multiple mechanisms of vaccine-mediated protection against SIV. Ackerman, ME, Das, J, Pittala, S, Broge, T, Linde, C, Suscovich, TJ, Brown, EP, Bradley, T, Natarajan, H, Lin, S et al.. 2018. Nat. Med. , .
    doi: 10.1038/s41591-018-0161-0PMID:30177821
  2. ADAM10 Sheddase Activity is a Potential Lung-Cancer Biomarker. Yoneyama, T, Gorry, M, Sobo-Vujanovic, A, Lin, Y, Vujanovic, L, Gaither-Davis, A, Moss, ML, Miller, MA, Griffith, LG, Lauffenburger, DA et al.. 2018. J Cancer 9, 2559-2570.
    doi: 10.7150/jca.24601PMID:30026855
  3. Exploiting glycan topography for computational design of Env glycoprotein antigenicity. Yu, WH, Zhao, P, Draghi, M, Arevalo, C, Karsten, CB, Suscovich, TJ, Gunn, B, Streeck, H, Brass, AL, Tiemeyer, M et al.. 2018. PLoS Comput. Biol. 14, e1006093.
    doi: 10.1371/journal.pcbi.1006093PMID:29677181
  4. The colonic epithelium plays an active role in promoting colitis by shaping the tissue cytokine profile. Lyons, J, Ghazi, PC, Starchenko, A, Tovaglieri, A, Baldwin, KR, Poulin, EJ, Gierut, JJ, Genetti, C, Yajnik, V, Breault, DT et al.. 2018. PLoS Biol. 16, e2002417.
    doi: 10.1371/journal.pbio.2002417PMID:29596476
  5. Interconnected Microphysiological Systems for Quantitative Biology and Pharmacology Studies. Edington, CD, Chen, WLK, Geishecker, E, Kassis, T, Soenksen, LR, Bhushan, BM, Freake, D, Kirschner, J, Maass, C, Tsamandouras, N et al.. 2018. Sci Rep 8, 4530.
    doi: 10.1038/s41598-018-22749-0PMID:29540740
  6. Inflammatory but not mitogenic contexts prime synovial fibroblasts for compensatory signaling responses to p38 inhibition. Jones, DS, Jenney, AP, Joughin, BA, Sorger, PK, Lauffenburger, DA. 2018. Sci Signal 11, .
    doi: 10.1126/scisignal.aal1601PMID:29511118
  7. In vivo systems biology approaches to chronic immune/inflammatory pathophysiology. Starchenko, A, Lauffenburger, DA. 2018. Curr. Opin. Biotechnol. 52, 9-16.
    doi: 10.1016/j.copbio.2018.02.006PMID:29494996
  8. Integrated in vivo multiomics analysis identifies p21-activated kinase signaling as a driver of colitis. Lyons, J, Brubaker, DK, Ghazi, PC, Baldwin, KR, Edwards, A, Boukhali, M, Strasser, SD, Suarez-Lopez, L, Lin, YJ, Yajnik, V et al.. 2018. Sci Signal 11, .
    doi: 10.1126/scisignal.aan3580PMID:29487189
  9. A Model of Dormant-Emergent Metastatic Breast Cancer Progression Enabling Exploration of Biomarker Signatures. Clark, AM, Kumar, MP, Wheeler, SE, Young, CL, Venkataramanan, R, Stolz, DB, Griffith, LG, Lauffenburger, DA, Wells, A. 2018. Mol. Cell Proteomics 17, 619-630.
    doi: 10.1074/mcp.RA117.000370PMID:29353230
  10. Increased Expression and Modulated Regulatory Activity of Coinhibitory Receptors PD-1, TIGIT, and TIM-3 in Lymphocytes From Patients With Systemic Sclerosis. Fleury, M, Belkina, AC, Proctor, EA, Zammitti, C, Simms, RW, Lauffenburger, DA, Snyder-Cappione, JE, Lafyatis, R, Dooms, H. 2018. 70, 566-577.
    doi: 10.1002/art.40399PMID:29245183
More Publications
Photo credit: Kathy Wittman