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Glycolytic phenotype and AMP kinase modify the pathologic response of tumor xenografts to VEGF neutralization

Giorgia Nardo1, Elena Favaro, Matteo Curtarello

  • 1Department of Oncology and Surgical Sciences, Oncology Section, University of Padova, Padova, Italy.

Cancer Research
|May 7, 2011
PubMed

Insights

Anti-VEGF therapy depletes tumor glucose and ATP, leading to necrosis and regression. This response involves AMP-activated protein kinase (AMPK) activation, offering potential predictive biomarkers for cancer treatment.

Area of Science:

  • Oncology
  • Metabolic Imaging
  • Cancer Therapeutics

Background:

  • Vascular Endothelial Growth Factor (VEGF) antagonists are established cancer therapies.
  • Predictive biomarkers for anti-VEGF therapy response and toxicity are currently lacking.

Purpose of the Study:

  • To investigate the impact of anti-VEGF therapy on tumor metabolism and therapeutic outcomes.
  • To identify potential imaging biomarkers for predicting response to anti-VEGF treatment.

Main Methods:

  • Utilized integrated imaging techniques: bioluminescence metabolic imaging, 18-fluorodeoxyglucose positron emission tomography (FDG-PET), and MRI.
  • Analyzed metabolic changes and their correlation with tumor response in preclinical cancer models.

Main Results:

  • Anti-VEGF therapy induced significant glucose depletion and ATP exhaustion in tumors, despite maintained glucose uptake.
  • Metabolic alterations correlated with increased tumor necrosis and partial regression, particularly in highly glycolytic tumors.
  • AMP-activated protein kinase (AMPK) was activated by anti-VEGF therapy; its attenuation exacerbated glucose consumption and necrosis.

Conclusions:

  • Established functional links between the Warburg effect, AMPK pathway, and therapeutic response to VEGF neutralization.
  • Findings suggest potential metabolic imaging biomarkers for predicting anti-VEGF therapy efficacy and toxicity.

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