Metabolism addiction in pancreatic cancer

被引:120
作者
Blum, R. [1 ,2 ]
Kloog, Y. [3 ]
机构
[1] NYU, Sch Med, Smilow Res Ctr, Dept Pathol, New York, NY 10016 USA
[2] NYU, Sch Med, Smilow Res Ctr, Inst Canc, New York, NY 10016 USA
[3] Tel Aviv Univ, Dept Neurobiol, IL-69978 Tel Aviv, Israel
基金
以色列科学基金会;
关键词
pancreatic cancer; oncogenic Ras; metabolism; glutamine metabolism; glycolysis; pentose phosphate pathway; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; ENDOTHELIAL GROWTH-FACTOR; RAS GENE-MUTATIONS; CELL-DEATH; LACTATE-DEHYDROGENASE; SIGNALING PATHWAY; ACTIVATED AKT; END-PRODUCTS; TUMOR-GROWTH; FACTOR-ALPHA;
D O I
10.1038/cddis.2014.38
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Pancreatic ductal adenocarcinoma, an aggressively invasive, treatment-resistant malignancy and the fourth leading cause of cancer deaths in the United States, is usually detectable only when already inevitably fatal. Despite advances in genetic screening, mapping and molecular characterization, its pathology remains largely elusive. Renewed research interest in longstanding doctrines of tumor metabolism has led to the emergence of aberrant signaling pathways as critical factors modulating central metabolic networks that fuel pancreatic tumors. Such pathways, including those of Ras signaling, glutamineregulatory enzymes, lipid metabolism and autophagy, are directly affected by genetic mutations and extreme tumor microenvironments that typify pancreatic tumor cells. Elucidation of these metabolic networks can be expected to yield more potent therapies against this deadly disease.
引用
收藏
页码:e1065 / e1065
页数:13
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