TY - JOUR
T1 - Metabolism addiction in pancreatic cancer
AU - Blum, R.
AU - Kloog, Y.
N1 - Funding Information:
Acknowledgements. We thank Ms. Shirley Smith for editorial assistance. This work was supported by an Israel Science Foundation Grant 06049200403 (YK), and by the Prajs-Drimmer Institute for the Development of Anti-Degenerative Disease Drugs (YK). YK is the incumbent of the Jack H Skirball Chair in Applied Neurobiology.
PY - 2014/2
Y1 - 2014/2
N2 - 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, glutamine-regulatory 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.
AB - 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, glutamine-regulatory 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.
KW - glutamine metabolism
KW - glycolysis
KW - metabolism
KW - oncogenic Ras
KW - pancreatic cancer
KW - pentose phosphate pathway
UR - http://www.scopus.com/inward/record.url?scp=84896778081&partnerID=8YFLogxK
U2 - 10.1038/cddis.2014.38
DO - 10.1038/cddis.2014.38
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AN - SCOPUS:84896778081
SN - 2041-4889
VL - 5
JO - Cell Death and Disease
JF - Cell Death and Disease
IS - 2
M1 - e1065
ER -