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Abstract #4044

Effect of PKM2 Activator and 2-Deoxyglucose Treatments on Cancer Metabolism Measured in vivo by hyperpolarized 13C MR Spectroscopic Imaging

Jae Mo Park 1 , Sui-Seng Tee 1 , Ralph Hurd 2 , Kyle Brimacombe 3 , Matthew Boxer 3 , Dirk Mayer 4 , Brian Rutt 1 , and Daniel Spielman 1

1 Radiology, Stanford University, Stanford, CA, United States, 2 GE Healthcare, Menlo Park, CA, United States, 3 National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, United States, 4 Diagnostic Radiology and Nuclear Medicine, University of Maryland, MD, United States

PKM2, the M2 isoform of pyruvate (Pyr) kinase, plays a role in the last step of glycolysis, converting phosphoenolpyruvate (PEP) to Pyr. So far, PKM2 is expressed in all tested cancer cells. We hypothesized that the use of a glucose analogue, 2-deoxyglucose (2DG), in combination with the PKM2 activator will accelerate the uptake of the toxic 2DG in tumors, and observed the therapeutic response in Pyr metabolism of tumor-bearing mice using hyperpolarized 13C Pyr MRSI. Lactate (Lac)-to-Pyr ratio consistently increased in all mice with dual-treatment while single treated mice did not. It suggests that there might be a synergic anti-cancer mechanism of the PKM2 activator and 2DG, and accelerates glucose starvation in tumors.

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