Wayne C. Glasgow, Ph.D.

  • GlasgowDirector, Curtis and Elizabeth Anderson Cancer Institute
    Department of Laboratory Oncology Research
    Associate Dean for Research, Professor and Chair, Department of Biomedical Sciences, Mercer University School of Medicine

    912-350-1707 (phone)
    GlasgWa1@memorialhealth.com


    Research Focus
    The role of bioactive lipids in the regulation of cell proliferation, differentiation, and transformation. In particular, research characterizes metabolites of arachidonic and linoleic acid as mediators of growth factor signal transduction with human breast, prostate, and colon cancer cells. Pharmacological modulation of these metabolic pathways may regulate the growth and metastatic potential of certain tumor cell types.

    Biography
    Wayne C. Glasgow, Ph.D., received a Bachelor of Science in Chemistry degree from the Georgia Institute of Technology and a Doctor of Philosophy in Pharmacology degree from Vanderbilt University. He completed post-doctoral training at the National Institutes of Health. Glasgow joined the faculty of Mercer University School of Medicine in 1996. In addition to serving as director of the laboratory oncology research program at the Anderson Cancer Institute, he serves as the associate dean for research and chair of the department of biomedical sciences at Mercer University School of Medicine. He has authored more than 50 publications in peer-reviewed research journals. Glasgow serves as study section member for the Department of Defense Breast Cancer Research Program and as a member of the Georgia Cancer Coalition Distinguished Cancer Clinicians and Scientists Executive Advisory Committee.

    Recent Publications
    Nony, P.A., Kennett, S.B., Olden, K., Roberts, J.D., and Glasgow, W.C. 15(S)-Lipoxygenase-2 mediates arachidonic acid-stimulated adhesion of human breast carcinoma cells through activation of TAK1, MKK6, and p38 MAPK. Journal of Biological Chemistry 280: 31413-31419, 2005.

    Moon, Y., Eling, T.E., and Glasgow, W.C. Curcumin suppresses interleukin 1-mediated microsomal prostaglandin E synthase-1 (mPGES-1) by altering early growth response gene EGR-1 and other signaling pathways. Journal of Pharmacology and Experimental Therapeutics 315: 788-795, 2005.

    Wang, Y., Zhang, W., Yang, Y., Sun, L., Chen, J., Fu, C., Hui, R., and Glasgow, W.C. VKORC1 Haplotype is associated with arterial vascular diseases (stroke, coronary heart disease, and aortic dissection). Circulation 113: 1615-1621, 2006.

    Bondesen, B., Glasgow, W.C., and Pavlath, G. Prostacyclin modulates muscle cell fusion. FASEB Journal 21: 3338-3345, 2007.

    Bajpai, A., Blaskova, E., Pakala, S.B., Glasgow, W.C., Penn, J.S., Johnson, D.A., and Rao, G.N. Hypoxia induces 15(S)-HETE production in human retinal microvascular endothelial cells: novel role for MEK1 in 15(S)-HETE-induced angiogenesis. Investigative Opthalmology and Visual Science 48: 4930-4938, 2007.

    Patulu, H.S.K., Wang, D., Quyen, D.V., Singh, N.K., Kudumani-Sridharan, V., Karpurapu, M., Park, E.A., Glasgow, W.C., and Rao, G. N. SRC-dependent STAT3-mediated expression of monocyte chemoattractant protein-1 is required for 15(S)-HETE-induced vascular smooth muscle migration. Journal of Biological Chemistry 284: 31142-31155, 2009.

    Chava, K.R., Karpurapu, M., Wang, D., Bhanoori, M., Kundumani-Sridharan, V., Zhang, Q., Ichiki, T., Glasgow, W.C., and Rao, G.N. CREB-mediated IL-6 expression is required for 15(S)-HEWTE induced vascular smooth muscle cell migration. Arteriosclerosis, Thrombosis, and Vascular Biology 29: 809-815, 2009.