Gregory A. Dekaban
Why I Became a Scientist
Growing up in the shadow of the National Institutes of Health (NIH) and The Bethesda Naval Medical Center, with a father, a clinician scientist in paediatric neurology at NIH, combined with a growing curiosity about all things biological and medical, I developed a natural inclination to become a scientist. So I did, without doubt or regret.
The research in my laboratory is centered in two major areas:
A focus of our research is to define the role of the CD11d CD18 integrin in leukocyte biology and inflammation of the central nervous system. Through the use of immunological, molecular and cell biological techniques, my laboratory is defining the phenotype and function of different monocyte subsets that infiltrate the central nervous system following traumatic injury. In addition, my laboratory is involved in developing a novel anti-inflammatory treatment for spinal cord injury that involves blocking leukocytes from infiltrating the site of injury from the blood.
The second focus on my research is the development of novel therapeutic vaccine approaches for cancer. The current emphasis is in developing dendritic cell-based therapeutic vaccines. The laboratory is working in collaboration with Dr. Paula Foster to develop real-time cellular magnetic resonance imaging techniques as a means to track dendritic cell migration in vivo in humans.
Why does inflammation develop throughout the body when the only injury is trauma to the spinal cord?
Although spinal cord injury (SCI) can have long lasting and devastating neurological consequences, treating acute systemic inflammation following SCI is often more critical to survival. That SCI can elicit such a systemic inflammatory response suggests that a level of communication and control exists between the immune system and the central nervous system. By understanding nature of the relationship between the central nervous system and the immune system it will become easier to develop therapeutics strategies to treat neurotrauma more effectively.
Why are vaccines against cancer an effective immunotherapy for a few individuals but not for most cancer patients.
It is critical to understand how best to design a cancer vaccine such that it recognizes only the tumor without inducing an equally destructive autoimmune response to normal issue. Furthermore tumors develop sophisticated ways of evading an immune response even in the face of an effective vaccine response. Thus, it is important to understand the nature of these tumor-specific immune evasion strategies. Through such an understanding it will be possible to block the tumor’s immune evasion strategy which in turn will result in the cancer patient responding more effectively to an anti-cancer immunotherapy.
- Honours B.Sc. in Biochemistry, Queen’s University
- Ph.D. in Biochemistry, University of Western Ontario
- Post-Doctoral training at the Frederick Cancer Research Facility
- National Cancer Institute of Canada Studentship
- Morris Kroll Memorial Scholarship for Cancer Research
- International Fogarty Post-Doctoral Fellowship
- Medical Research Council of Canada Post-Doctoral Fellowship
- Ontario Ministry of Health Career Scientist Award
- Ontario Ministry of Health Career Scientist Award, renewed
- University of Western Ontario President’s Occupational Health and Safety Award
Bao, F., Bailey, C.S., Gurr, K.R., Bailey, S.I., Rosas-Arellano, M.P., Dekaban, G.A., and Weaver, L.C. Increased oxidative activity in human blood neutrophils and monocytes after spinal cord injury. Experimental Neurology 2009 215: 308-316. epub 2008/11/13.
Dekaban, G.A.*, Snir, J., Shrum, B., de Chickera, S., Willert, C., Said E.A., Sékaly, R.P., Foster, P.J. and O’Connell, P.J.* Semi-quantitation of mouse dendritic cell migration in vivo using cellular MRI. J. Immunotherapy, 32: 240-251 (2009) PMID: 19242346. * Co-senior authors.
Bao, F., Bailey, C.S., Gurr, K.R., Bailey, S.I., Rosas-Arellano, M.P., Brown, A., Dekaban, G.A. and Weaver, L.C. Human spinal cord injury causes specific increases in surface expression of Beta integrins on leukocytes. J. Neurotrauma. 2011: 28:269-280.
Bao, F., Brown, A., Dekaban, G.A., Omaña, V. and Weaver, L.C. Anti-CD11d integrin blockade reduces the systemic inflammatory response syndrome after spinal cord injury. Expt. Neurology (2011) 231: 272-283.
Zhang, X, de Chickera, S.N., Willert, C., Economopoulos, V., Noad, J., Rohani, R., Wang, A.Y., Leving, M.K., Scheid, E., Foley, R., Foster, P.J. and Dekaban, G.A. Non-invasive detection of the in vivo migration of human monocyte-derived dendritic cells into the popliteal lymph nodes of CB17/scid mouse with cellular MRI. Cytotherapy. (2011) 13:1234-1248.
*de Chickera, S.N., *Willert, C., Noad, J., Mallett, C., Foster, P.J. and Dekaban, G.A. Cellular MRI as a sensitive, non-invasive modality suitable for detecting differences between the migratory efficiencies of different DC populations in vivo. International Immun. (2011) 24: 29-41.
Mawhinney, L.A., *Thawer, S., Lu, W.-Y., van Roojen, N., Weaver, L.C., Brown, A. and Dekaban, G.A. Differential detection and distribution of microglial and hematogenous macrophage populations in the injured spinal cord of the lys-EGFP-ki transgenic mouse. J Neuropathol Exp Neurol. (2012) 71: 180-197.
Gregory A. Dekaban, Ph.D.
Scientist, BioTherapeutics Research Laboratory
Director, Molecular Medicine
Robarts Research Institute, Room 2214
1151 Richmond Street, North
N6A 5B7 CANADA
Phone: 519-931-5777 ext. 24241
Administrative Assistant: Ilda Moniz