Abstract #0581

Glutamine Metabolism Dysregulated in PDAC induced Cachexia

Santosh Kumar Bharti¹, Paul T Winnard¹, Raj Kumar Sharma¹, Yelena Mironchik¹, Michael Gilbert Goggins^2,3,4, and Zaver M. Bhujwalla^1,5,6

¹Division of Cancer Imaging Research, The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ²Department of Medicine - Gastroenterology and Hepatology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ³Department of Oncology-Gastrointestinal Cancer, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁴Department of Pathology-Gastroenterology and Liver Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁵Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁶3Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States

Glutamine is one of the most abundant circulating amino acids that is critical for many fundamental functions in cancer cells, including synthesis of metabolites that maintain mitochondrial metabolism, protein synthesis, acting as a carbon source or as the primary nitrogen donor for multiple essential biosynthetic pathways, and in the activation of cell signaling. Here we have identified significant differences in glutamine in human plasma from pancreatic cancer patients that were also observed in tumor interstitial fluid from pancreatic cancer xenografts that induced cachexia. These results suggest that agents with glutaminolytic activity may be useful in treating cachexia.

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