The biology of cancer: metabolic reprogramming fuels cell growth and proliferation
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TLDR
This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types and regulates regulation of these fluxes by cellular mediators of signal transduction and gene expression.About:
This article is published in Cell Metabolism.The article was published on 2008-01-01 and is currently open access. It has received 3526 citations till now. The article focuses on the topics: PI3K/AKT/mTOR pathway & Lipid biosynthesis.read more
Citations
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The autophagy conundrum in cancer: influence of tumorigenic metabolic reprogramming
TL;DR: How metabolic reprogramming influences autophagic activity in tumors is reviewed, and how inhibition of autophagy might be exploited to target tumor cells that show altered metabolism is discussed.
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Reversing the Warburg effect as a treatment for glioblastoma.
Ethan Poteet,Gourav Roy Choudhury,Ali Winters,Wenjun Li,Myoung-Gwi Ryou,Ran Liu,Lin Tang,Anuja Ghorpade,Yi Wen,Fang Yuan,Stephen T. Keir,Hai Yan,Darell D. Bigner,James W. Simpkins,Shao-Hua Yang,Shao-Hua Yang +15 more
TL;DR: It is documented that methylene blue reverses the Warburg effect evidenced by the increasing of oxygen consumption and reduction of lactate production in GBM cell lines.
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Molecular Pathways: Targeting Cellular Energy Metabolism in Cancer via Inhibition of SLC2A1 and LDHA
Aik Ooi,Brigitte N. Gomperts +1 more
TL;DR: Results indicate that disrupting SLC2A1, LDHA, or other regulators in cancer cell energetics is a very promising approach for new targeted therapies.
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Current Scientific Rationale for the Use of Somatostatin Analogs and mTOR Inhibitors in Neuroendocrine Tumor Therapy
Corinne Bousquet,Charline Lasfargues,Mounira Chalabi,Siham Moatassim Billah,Christiane Susini,Delphine Vezzosi,Philippe Caron,Stéphane Pyronnet +7 more
TL;DR: The scientific rationale for the potential additive or synergistic antitumor effects of combined therapy of somatostatin analogs and everolimus offers a promising treatment option for neuroendocrine tumors.
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Neural stem/progenitor cells display a low requirement for oxidative metabolism independent of hypoxia inducible factor‐1alpha expression
TL;DR: Data indicate that NSPCs have a relatively low requirement for oxidative metabolism for their survival and that hypoxic resistance is not dependent upon HIF‐1α signaling.
References
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Dennis J. Slamon,William Godolphin,Lovell A. Jones,John A. Holt,Steven G. Wong,Duane E. Keith,Wendy J. Levin,Susan G. Stuart,Judy Udove,Axel Ullrich,Michael F. Press +10 more
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TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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High frequency of mutations of the PIK3CA gene in human cancers
Yardena Samuels,Zhenghe Wang,Alberto Bardelli,Natalie Silliman,Janine Ptak,Steve Szabo,Hai Yan,Adi F. Gazdar,Steven M. Powell,Gregory J. Riggins,James K V Willson,Sanford D. Markowitz,Kenneth W. Kinzler,Bert Vogelstein,Victor E. Velculescu +14 more
TL;DR: To determine if PI3Ks are genetically altered in tumorigenesis, they were sequenced in human for the first time and the results allowed us to assess the importance of phosphatidylinositol 3-kinases in neoplasia.
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HIF-1-mediated expression of pyruvate dehydrogenase kinase: A metabolic switch required for cellular adaptation to hypoxia
TL;DR: A hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production is revealed.