Glucose Oncometabolism of Esophageal Cancer

Author(s): Jason S. Hochwald, Jianliang Zhang

Journal Name: Anti-Cancer Agents in Medicinal Chemistry
(Formerly Current Medicinal Chemistry - Anti-Cancer Agents)

Volume 17 , Issue 3 , 2017

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Graphical Abstract:


Metabolic reprograming contributes to esophageal tumorigenesis. A better understanding of how esophageal cancer (EC) cells reactivate primitive signaling to retain glucose metabolism under unfavorable conditions is essential for the development of therapeutic interventions to treat EC. Current achievements in the field of EC glucose metabolism have been critically reviewed to address several fundamental questions. These include: 1) the association of abnormal glucose metabolism and EC risk; 2) alterations of genes and/or proteins that contribute to glucose oncometabolism in EC; 3) signal transduction pathways that promote EC consumption of glucose; and, 4) targeting the glycolytic element or the EC dependency on excessive glucose consumption to prevent growth of EC caused by different genomic changes.

Keywords: Tumor metabolism, glycolysis, mitochondria, altered genes, inhibitors, glucose dependence.

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Article Details

Year: 2017
Published on: 19 February, 2017
Page: [385 - 394]
Pages: 10
DOI: 10.2174/1871520616666160627092716
Price: $65

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