How cancer metabolism is tuned for proliferation and vulnerable to disruption
By A. Schulze, Adrian L. Harris. Nature, 2012
878 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/bd4b22160c23fb26ad17be5d2f8a1df02ec61f68
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- Navdeep S. Chandel
- Ralph J. Deberardinis
- Craig B. Thompson
- E. White
- Joshua D. Rabinowitz
- A. Schulze
- N. Hay
- Ajla T. Wasti
In Molecular Biology
- Ralph J. Deberardinis
- Navdeep S. Chandel
- E. White
- Craig B. Thompson
- Joshua D. Rabinowitz
- T. Walther
- Robert V Farese
- A. Schulze
Citations in the corpus
- Cholesteryl Ester Accumulation Induced by PTEN Loss and PI3K/AKT Activation Underlies Human Prostate Cancer Aggressiveness (2014, background): “Cancer cells adopt metabolic pathways that differ from their normal counterparts by high rates of glycolysis and biosynthesis of essential macromolecules to fuel rapid growth (Schulze and Harris, 2012).”
- Glutamine and cancer: cell biology, physiology, and clinical opportunities. (2013, background): “Introduction It has been nearly a century since the discovery that tumors display metabolic activities that distinguish them from differentiated, non-proliferating tissues and presumably contribute to their supraphysiological survival and growth (1).”
- Hypoxic and Ras-transformed cells support growth by scavenging unsaturated fatty acids from lysophospholipids (2013, background): “Whereas tumors driven by the PI3K-Akt pathway wantonly engage in biosynthesis and become metabolically vulnerable (38), those driven primarily by oncogenic Ras instead have the capacity to maintain rapid growth by using extracellular macromolecules to obtain the required substrates for new macromole”
- Cellular Fatty Acid Metabolism and Cancer (2013, background): “A better understanding of these metabolic changes has prompted new approaches toward cancer therapy (reviewed in Hsu and Sabatini, 2008; Schulze and Harris, 2012).”
- Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, background): “The elevated glucose metabolism is required to provide sufficient amounts of metabolic intermediates to support anabolic processes, such as nucleic acid, lipid, and protein synthesis in the rapidly dividing cancer cells (for review, see Lunt and Vander Heiden, 2011; Schulze and Harris, 2012).”
- Tumor-derived hydrogen sulfide, produced by cystathionine-β-synthase, stimulates bioenergetics, cell proliferation, and angiogenesis in colon cancer (2013, background): “Tumor bioenergetics relies both on oxidative phosphorylation, as well as glycolysis (even in the presence of normal oxygen supply, a phenomenon known as the Warburg effect) (16, 17).”