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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