MSRD 2016 Sample Abstract
Your abstract MUST be in the following format:
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2. TITLE must be CAPITALIZED and bolded
3. Author names should be written as 1st initial followed by period, and then
Last Name (ex: Jane Jaime Doe  J. J. Doe)
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5. Name of presenting student should be bolded
6. Abstract must have the following headings CAPITALIZED and bolded:
INTRODUCTION (or BACKGROUND), OBJECTIVE, METHODS,
RESULTS, and CONCLUSION (or DISCUSSION). If you believe your
research is best presented in an unstructured abstract format you may submit
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names and affiliations, subheadings from point 6 above, and the research)
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MSRD 2016 Abstract”
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MASS SPECTROMETRY-BASED PHOSPHOLIPIDOMICS OF ONCOLYTIC VIRUSINFECTED LEUKEMIA CELLS
M. Atkins1,2, C. Canez2, J. Hajjar3, G. Waghray3, H. Atkins3, and J. C. Smith2
1MD/PhD
Program, University of Toronto, Toronto, Ontario, Canada 2Department of
Chemistry, Carleton University, Ottawa, Ontario, Canada and 4Centre for Innovation in
Cancer Therapeutics, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada
BACKGROUND/PURPOSE: Oncolytic viruses (OVs) are effective therapeutic agents that
selectively target cancer cells. However, many of the molecular mechanisms of infection
remain unresolved. Understanding the cellular response to infection will inform the design
of sensitizers that improve OV efficacy. Lipid signaling and cellular metabolism have
recently emerged as targets of non-OV infection to expand cell membranes, alter
membrane curvature and fluidity and act as signaling molecules, but their role in OV
infection is unknown. We examine the cellular response to two OVs, VSV and a
corresponding mutant, VSV-Δ51M in leukemic cells. OBJECTIVES: We seek to
understand early lipid regulation of cancer cells to OV infection. METHODS: Our online
liquid chromatography-mass spectrometry approach identified 168 phosphatidylcholine
(PC) lipids using a positive ion mode precursor ion scan for m/z 184. Moreover, a negative
ion mode precursor ion scan for m/z 168 was used to discriminate sphingomyelin (SM)
from PC. RESULTS: SMs are unchanged in the early cellular response to OV infection. In
contrast, PCs are dysregulated in the early cellular response to OV infection. Low m/z PCs
are down-regulated and high m/z PCs are up-regulated, which suggests OV infection
targets the conversion of lysophosphatidylcholine (LPC) lipids to diacylphosphatidylcholine
(DPC) lipids. We have identified LPCAT2 as a potential target of OV infection that regulates
lipid metabolism. CONCLUSIONS: Our LC-MS approach suggests the early cellular
response to OV infection is not mediated through SMs, but DPCs are up-regulated at the
expense of LPCs soon after OV infection. We next seek to understand the subcellular
regulation of phospholipids, which will facilitate the identification of candidate protein
regulators.