|Rosalind and Morris Goodman Cancer Centre and the Department of Physiology |
Life Sciences Complex (Cancer Pavilion)
Office: Room 613
Lab: Room 603b
1160 Avenue Des Pins Ouest
H3G 0B1 Canada
Laboratory web site:
Research Area: Immunology, Molecular and Cell Biology
My laboratory is interested in studying the molecular mechanisms underlying cellular growth and proliferation, and how these processes are normally regulated in the immune system or deregulated during tumourigenesis. My research centers on understanding how biological systems coordinate their metabolic activities to meet the bioenergetic challenges of proliferation. During proliferation a mother cell must increase its biomass and replicate its genome prior to dividing to create two daughter cells. Thus, the decision to proliferate presents a significant bioenergetic challenge – the cell must generate enough energy and acquire or synthesize biomolecules at a sufficient rate to meet the demands of proliferation. One of the intriguing problems in biology is understanding the mechanisms by which cells adapt to survive periods of metabolic stress and maintain cell growth and proliferation. Tumour cells often display fundamental changes in energy metabolism and increase their uptake of nutrients such as glucose to meet the increased bioenergetic demands of proliferation.
Future studies in my lab will focus on elucidating the critical interactions between signal transduction pathways and cellular metabolism. Of particular interest is the function of the AMP-activated protein kinase (AMPK), a critical regulator of cellular metabolism, and the tumour suppressor p53 in the cellular adaptation to metabolic stress. We will employ a variety of tools including biochemistry, metabolic analysis, cell biology, bioinformatics, and mouse models to address our biological questions. My hope is that by understanding the metabolic networks at play in both normal and pathological settings (i.e. cancer) we may gain insight that will lead to novel therapeutics for the treatment of cancer.
Education: Ph.D., Toronto
Jones, R.G., Bui, T., White, C., Muniswamy, M., Krawczyk, C.M., Frauwirth, K.A., Lindsten, T., Hawkins, B.J., Kubek, S., Wang, Y.L., Conway, S., Roderick, H.L., Bootman, M.D., Shen, H., Foskett, J.K., and Thompson, C.B. (2007). The proapoptotic factors Bax and Bak regulate T Cell proliferation through control of endoplasmic reticulum Ca(2+) homeostasis. Immunity 27(2):268-280.
Buzzai, M., Jones, R.G., Amaravadi, R.K., Lum, J.J., DeBerardinis, R.J., Zhao, F., Viollet, B., and Thompson, C.B. (2007). Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth. Cancer Res 67(14): 6745-6752.
Liu, L., Cash, T.P., Jones, R.G., Keith, B., Thompson, C.B., and Simon, M.C. (2006). Hypoxia-induced energy stress regulates mRNA translation and cell growth. Mol Cell 21: 521-531.
Jones, R.G., Plas, D.R., Kubek, S., Buzzai, M., Mu, J., Xu, Y., Birnbaum, M.J., and Thompson, C.B. (2005). AMP-activated protein kinase induces a p53-dependent metabolic checkpoint. Mol Cell 18(3): 283-293.