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  3. Susan Hockfield
Hockfield, Susan 150707 color resized.jpg
Hockfield
Susan
Ph.D.
President Emerita and Professor of Neuroscience
Brain & Cognitive Sciences
Faculty Appointment
Primary
Building
76-461
Email
hockfield@mit.edu
Phone
6172537284
    About

    President Emerita Susan Hockfield has retired from active research and is no longer accepting students or research staff.

    Susan Hockfield has distinguished herself in a career that has spanned advanced scientific research and the presidency of one of the premier institutions of science and engineering in the world.

    After earning a B.A. in biology from the University of Rochester and a Ph.D. from Georgetown University at the School of Medicine, Dr. Hockfield was an NIH postdoctoral fellow at the University of California at San Francisco. She then joined the scientific staff at the Cold Spring Harbor Laboratory in New York. Joining the faculty of Yale University in 1985, Dr. Hockfield focused her research on the development of the brain and on glioma, a deadly form of brain cancer, and pioneered the use of monoclonal antibody technology in brain research. She gained tenure in 1994 and was later named the William Edward Gilbert Professor of Neurobiology.

    At Yale, Dr. Hockfield emerged as a strong, innovative university leader, first as dean of its Graduate School of Arts and Sciences, with oversight of more than 70 graduate programs, and then as provost, Yale’s chief academic and administrative officer.

    From December 2004 through June 2012, Dr. Hockfield served as the sixteenth president of MIT, where she continues to hold a faculty appointment as professor of neuroscience.

    Research

    My laboratory has studied molecular substrates of mammalian development. We identified a family of glycovariants of the extracellular matrix (ECM) proteoglycan, aggrecan, whose expression is regulated by neuronal activity early in an animal's life. Expression of the aggrecan glycoforms is regulated in parallel with critical period events and may play a role in stabilizing mature synaptic relationships. A related ECM protein, BEHAB/brevican, is expressed when glial cells travel during development and after brain injury. BEHAB/brevican is also expressed at very high levels in brain tumors, and can mediate the motility of tumor cells. A key feature of our work has been to bring biochemical and molecular biological techniques to the classical anatomical analysis of mammalian CNS development.

    Publications

    Hockfield S. The next innovation revolution. Science. 2009 Feb 27;323(5918):1147.

    Viapiano MS, Hockfield S, Matthews RT. BEHAB/brevican requires ADAMTS-mediated proteolytic cleavage to promote glioma invasion. J Neurooncol. 2008 Jul;88(3):261-72. Epub 2008 Apr 9.

    Viapiano MS, Bi WL, Piepmeier J, Hockfield S, Matthews RT. Novel tumor-specific isoforms of BEHAB/brevican identified in human malignant gliomas. Cancer Res. 2005 Aug 1;65(15):6726-33.

    Viapiano MS, Matthews RT, Hockfield S. A novel membrane-associated glycovariant of BEHAB/brevican is up-regulated during rat brain development and in a rat model of invasive glioma. J Biol Chem. 2003 Aug 29;278(35):33239-47. Epub 2003 Jun 10.

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