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Isa  M.  Hussaini
Degree(s): Ph.D.
Graduate School: King’s College, University of London
Primary Appointment: Associate Professor of Pathology
Research Interests:
The Roles of PKC-eta and LRP in Glioblastoma Invasive Growth

Email Address: imh5c@virginia.edu
Biomedical Sciences Graduate Program(s)
  • Molecular Medicine
  • Neuroscience
  • Biochemistry, Molecular Biology and Genetics
    • Research Description

    The prognosis for patients with malignant astroglial tumors is poor. The capacity of astrocytomas both to invade adjacent brain sites and to migrate into distant ones precludes curative surgical resection; and little progress has been made in designing adjuvant therapies that significantly affect long-term survival. In order to formulate more novel therapeutic strategies, it is essential to have a better understanding of how the invasive growth of these tumors is controlled. The primary interest of the laboratory is the regulation of LRP (low density lipoprotein receptor-related protein) expression and function in astrocytic tumor cells. LRP is an endocytic receptor involved in the trafficking of a variety of protein/protein complexes that have pathophysiologic relevance in the central nervous system, including urokinase (uPA) and its receptor (uPAR), lipoprotein metabolites, and activated alpha2-macroglobulin. Changes in LRP expression may regulate the levels of modulators (uPA, uPAR and PAI-1) of migration/invasion around the microenvironment of astrocytic tumors. The second project in my laboratory focuses on understanding differences in PKC-eta activation and expression between malignant vs. non-neoplastic astrocytes and on the role of PKC-eta in the control of cell proliferation and apoptosis. The regulation of cell proliferation and apoptosis in malignant astrocytic tumors is undoubtedly complex; however, we are investigating how PKC-eta regulation of these processes may be exploited to provide an experimental system in which proliferative or apoptotic phenotype may be selectively induced and studied. We are also extrapolating some of our results in cultured cells to glioblastoma animal models. We hypothesize that pharmacological regulation of PKC-eta, in combination with drugs targeting cellular migration, may present a new therapeutic paradigm for these aggressive brain tumors.

    Selected Publications
  • Amos S, Martin PM, Polar GA, Parsons SJ and Hussaini IM (2005). Phorbol 12-myristate 13-acetate induces epidermal growth factor receptor transactivation via protein kinase C delta/c-Src pathways in glioblastoma cells. J Biol Chem. 280(9):7729-38.
  • Martin P.M and Hussaini, I M (2005) PKC-h as a Therapeutic Target in glioblastoma Multiforme, (Review) Expert Opinion in Therapeutic Targets 9(2): 299-313.
  • Aeder, SE, Martin P.M, Soh J-W and Hussaini, IM (2004) PKC-h Mediates Glioblastoma Proliferation via the Akt and mTOR Signaling Pathways. Oncogene 23:9062-9069.
  • Hussaini, IM, Karns, LR, Griffith, V, Carpenter, JE, Redpath, GT, Sando, JJ and VandenBerg, SR (2000). Phorbol 12-myristate-13-acetate induces protein kinase C-h-specific proliferative response in astrocytic tumor cells. J. Biol. Chem. 275: 22348-22354.
  • PubMed Listings for this Faculty Member
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    Contact Information
      Office Address: PO Box 800904, MR 5 Room 3324, 415 Lane Road, 
      Office Phone: +1 434-924-0110, +1 434-924-9189
      Fax Phone: +1 434-924-2151
      Home Phone: +1 434-964-1718
      Web Site: http://www.healthsystem.virginia.edu/intern

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