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Rosalind A. Segal, MD, PhD

Pediatric Hematology/Oncology

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Rosalind A. Segal, MD, PhD


  • Edward J. Benz Jr., MD, Chair
  • Professor of Neurobiology, Harvard Medical School

Clinical Interests

  • Brain tumors
  • Pediatric brain tumors

Contact Information

  • Office Phone Number617-632-4737
  • Fax617-394-2936


Dr. Segal received her PhD in 1985 from Rockefeller University and her MD in 1986 from Cornell University Medical College, followed by a residency in the Harvard Neurology Program. As a postdoctoral fellow at Massachusetts Institute of Technology, she investigated the role of nerve growth factors in regulating cerebellar development and tumor formation. She joined DFCI in 1998, where she is principally involved in laboratory research on nervous system development.

Recent Awards:

  • National Merit Scholarship 1975
  • National Science Foundation Pre-doctoral Fellowship 1979
  • Phi Beta Kappa, Harvard College 1979
  • Summa Cum Laude, Harvard University 1979
  • Medical Science Training Program Pre-doctoral Fellowship 1980
  • Dana Foundation Postdoctoral Fellowship 1990
  • Robert Ebert Clinical Scholar Klingenstein Award 1996
  • Claudia Adams Barr Investigator, Barr Foundation 1998
  • Pediatric Brain Tumor Foundation Award 2001
  • McDonnell Foundation Award 2001
  • NIH Director's Pioneer Award 2006
  • Ted Williams Senior Investigator, Dana-Farber Cancer Institute 2009
  • American Association of Physicians 2011


Growth Factors in Central Nervous System Development and Oncogenesis

Our lab is interested in mechanisms whereby extracellular stimuli regulate proliferation and survival in the developing nervous system.

Neurotrophin Signaling

In order for target-derived neurotrophins to regulate the survival of a developing presynaptic cell, a signal must be propagated from the nerve terminal along the axon to the nucleus. We found that activated Trk receptors function as rapid retrograde signal carriers to elicit nuclear responses to target derived neurotrophins. Our data indicate that the mechanism of signal propagation is retrograde vesicular transport of activated Trk-ligand complexes. Once they reach the cell body, activated receptors elicit nuclear responses-including phosphorylation of the transcription factor CREB and subsequent induction of the immediate early gene c-fos.

We are currently studying other intermediates required for retrograde signaling and the potential differences in the biological responses to retrograde or local stimulation with growth factors.

Neurotrophins & Cancer

While our studies have highlighted the role of BDNF in normal cerebellar development, we have also demonstrated that neurotrophins, in particular NT3, have a role in cerebellar diseases.

Unregulated growth of cerebellar granule neuronal precursors results in formation of a tumor, known as medulloblastoma. We have found the NT3 receptor TrkC is expressed in these tumors, and that the level of expression is a prognostic indicator for clinical progression. Furthermore, our data show that NT3 induces an apoptotic response in medulloblastoma tumor cells, indicating that neurotrophins have potential application in tumor therapy.

Cerebellar Development

While target derived neurotrophins are required for the survival of developing neurons in the peripheral nervous system, the functions of neurotrophins in the central nervous system have been unclear. Mice with a targeted gene deletion of brain-derived neurotrophic factor (BDNF) exhibit a wide based gait, and a defect in cerebellar foliation pattern. At the cellular level cerebellar granule cell survival and migration are both impaired in mutant animals. However, there is an increase in granule cell proliferation in mutants. These data suggest that BDNF acts as an autocrine/paracrine factor to regulate survival, migration, and differentiation of developing CNS neurons, and thereby affects neural patterning.


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