Rosalind and Morris Goodman Cancer Centre and
Department of Physiology
Life Sciences Complex (Cancer Pavilion)
Office: Room 613
Lab: Room 603b
1160 Avenue Des Pins Ouest
H3G 0B1 Canada
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.
Jones, R.G., and Thompson, C.B. (2007).
Revving the engine: signal transduction fuels T cell activation.
Immunity 27(2): 173-178.
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
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.
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