I provideoversight for all industry-sponsored and investigator-initiated oncologyclinical research at Ochsner. I also oversee Ochsner’s Biorepository and theOchsner Center for Outcomes Research. Before I transitioned to anadministrative position, I was the head of the Laboratory for Cancer andDevelopmental Cell Biology at Van Andel Research Institute in Grand Rapids, Mi.My research interests focused on MEK signaling in health and disease.
EDUCATION/TRAINING (Beginwith baccalaureate or other initial professional education, such as nursing,include postdoctoral training and residency training if applicable. Add/deleterows as necessary.)
Queen’s University, Kingston, Ontario, Canada
BSc (Hons.)
05/1987
Biology
University of Toronto, Toronto, Ontario, Canada
MSc
09/1990
Zoology/Dev. Biology
University of Toronto, Toronto, Ontario, Canada
PhD
03/1996
Zoology/Dev. Biology
National Cancer Institute, Post-Doctoral Fellowship, Frederick, Maryland, USA
03/1999
Molecular Oncology
https://orcid.org/0000-0002-5708-4984
https://www.ncbi.nlm.nih.gov/myncbi/16gyk9zrtYSk9/bibliography/public/
SelectedPublications
Lee,C-S, Dykema, KJ, Hawkins, DM, Cherba, DM, Webb, CP, Furge, KA, and Duesbery,NS. 2011. Mitogen-activated proteinkinase kinase 2 is sufficient but not necessary for proliferation andanchorage-independent growth of SK-MEL-28 melanoma cells. PLoS One, 6(2): e17165. doi:10.1371/journal.pone.0017165.
Bromberg-White,JL, Boguslawski, EA, Hekman, D, Kort, EJ, and Duesbery, NS. 2011. Persistent Inhibition of Oxygen-InducedRetinal Neovascularization by Anthrax Lethal Toxin. I.O.V.S. 52(12), 8979-8992.
Ding,Y., E.A. Boguslawski, B.D. Berghuis, J.J. Young, Z. Zhang, K. Hardy, K. Furge,E. Kort, A.E. Frankel, R.V. Hay, J.H. Resau, and N.S. Duesbery. 2008. Mitogen-activated protein kinase kinase signaling promotes growth andvascularization of fibrosarcoma. Mol.Cancer Ther. 7(3): 648–658.
Young,J.J., J.L. Bromberg-White, C. Zylstra, J.T. Church, E. Boguslawski, J.H. Resau,B.O. Williams, and N.S. Duesbery. 2007. LRP5 and LRP6 are notrequired for protective antigen-mediated internalization or lethality ofanthrax lethal toxin. PLoS Path. 3(3):e27. PMC180872.
Abi-Habib,R.J., J.O. Urieto, S. Liu, S.H. Leppla, N.S. Duesbery, and A.E. Frankel.2005. BRAF status and mitogen-activatedprotein/extracellular signal–regulated kinase kinase 1/2 activity indicatesensitivity of melanoma cells to anthrax lethal toxin. Mol. Cancer Ther. 4(9): 1303–1310.
Liang,X., J.J. Young, S.A. Boone, D.S. Waugh, and N.S. Duesbery. 2004. Involvement of domain II in toxicity of anthrax lethal factor. J. Biol. Chem. 279(50): 52473–52478.
Chopra,A.P., X. Liang, S. Boone, and N.S. Duesbery. 2003. Anthrax lethal factorproteolysis and inactivation of MAP-kinase-kinase. J. Biol. Chem. 278(11): 9402–9406.
Koo,H.-M., M. VanBrocklin, M.J. McWilliams, S.H. Leppla, N.S. Duesbery, and G.F. VandeWoude. 2002. Apoptosis and melanogenesis in human melanomacells induced by anthrax lethal factor inactivation of mitogen-activatedprotein kinase kinase. Proc. Natl. Acad. Sci. U.S.A. 99(5):3052–3057. PMC122471.
Duesbery,N.S., J. Resau, C.P. Webb, S. Koochekpour, H.-M. Koo, S.H. Leppla, and G.F.Vande Woude, G.F. 2001. Suppression of ras-mediated transformationand inhibition of tumor growth and angiogenesis by anthrax lethal factor, aproteolytic inhibitor of multiple MEK pathways. Proc. Natl. Acad. Sci. U.S.A. 98(7): 4089–4094. PMC31184.
Duesbery,N.S., C.P. Webb, S.H. Leppla, V.M. Gordon, K.R. Klimpel, T.D. Copeland, T.D.,N.G. Ahn, M. Oskarsson, K. Fukasawa, K.D. Paull, and G.F. Vande Woude. 1998. Proteolytic inactivation of MAP-kinase kinaseby anthrax lethal factor. Science 280(5364): 734–737.
https://research.ochsner.org/clinical-research
Keywords:Clinical Research, Outcomes Research, Biorepository, Oncology
