title: Glucose Oncometabolism of Esophageal Cancer.
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.
authors.forename: Jason S
authors.initials: JS
authors.lastname: Hochwald
authors.affiliation: Department of Surgical Oncology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, United States.
authors.forename: Jianliang
authors.initials: J
authors.lastname: Zhang
mesh_terms: D004938:Esophageal Neoplasms / Q000378:metabolism* / Q000473:pathology; D005947:Glucose / Q000378:metabolism*; D006801:Humans
chemical_list: D005947:Glucose
keywords: Tumor metabolism; altered genes; glucose dependence; glycolysis; inhibitors; mitochondria