Purpose of Review Pancreatic adenocarcinoma is a leading cause of cancer mortality in western countries with a uniformly poor prognosis. Unfortunately, there has been little in the way of novel therapeutics for this malignancy over the last several decades. Derangements in metabolic circuitry favoring excess glycolysis are increasingly recognized as a key hallmark of cancer. Recent Findings The role of alterations in glutamine metabolism in pancreatic tumor progression has been elucidated in animal models and human cells lines, and there has been considerable interest in exploiting these aberrations for the treatment of pancreatic cancer. Other strategies targeting NQO1/GLS1 inhibition, NAD+ synthesis, and TCA cycle intermediates are being actively studied in the clinic. Summary Aberrant metabolism in pancreatic cancer poses a unique therapeutic strategy. We review preclinical and clinical studies looking to exploit alterations in the metabolic circuitry of pancreatic cancer. . . . . Keywords Pancreatic cancer Glutamine Anaplerosis NADPH-quinone oxidoreductase 1 ß-lapachone Abbreviations ROS Reactive oxygen species α-KG α-Ketoglutarate TCA Tricarboxylic acid cycle β-lap β-Lapchone BPTES Bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2- yl)ethyl sulfide Introduction Gln Glutamine GlnI Glutamine synthase Pancreatic adenocarcinoma (PDAC) is a leading cause of Gls1 Glutaminase 1 cancer-related mortality in western countries. In the USA, Gls2 Glutaminase 2 there
Current Oncology Reports – Springer Journals
Published: May 11, 2018
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