Regulation of cancer cell metabolism
By R. Cairns, I. Harris, T. Mak. Nature Reviews. Cancer, 2011
4,678 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9d36b5b10983f1aa90a9d9d5a7bcffe671b38257
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
- M. V. Vander Heiden
- A. Mayer
- Navdeep S. Chandel
- Joshua D. Rabinowitz
- David M. Sabatini
- J. Cantor
- Adrian L. Harris
- Jason W. Locasale
In Molecular Biology
- M. V. Vander Heiden
- Navdeep S. Chandel
- David M. Sabatini
- J. Cantor
- Joshua D. Rabinowitz
- Jason W. Locasale
- E. Panieri
- M. Santoro
Citations in the corpus
- ROS homeostasis and metabolism: a dangerous liason in cancer cells (2016, background): “enzyme-catalyzed reactions culminating in the generation of pyruvate, adenosine tris-phosphate (ATP) and reduced cofactors in the form of NADH.(71) As already observed by”
- Anoikis molecular pathways and its role in cancer progression. (2013, background): “take through PI3K/Akt pathway activation, quench ROS increasing NADPH production, rescuing cells from anoikis [35,189].”
- The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, background): “One can envision the possibility that growing mammalian cells, including cancer cells, could also in some circumstances need ribose 5-phosphate in excess of NADPH, i.e. when DNA and RNA nucleotide synthesis is maximized (Ferreira, 2010; Cairns et al., 2011).”
- Glutaminolysis: A Hallmark of Cancer Metabolism. (2017, background): “Knockdown of ME1 significantly lowers cellular NADPH/NADP+ in conjunction with clonogenic survival of pancreatic ductal adenocarcinoma cells (64, 90).”
- BCL-2 inhibition targets oxidative phosphorylation and selectively eradicates quiescent human leukemia stem cells (2013, background): “Cancer cells appear to commonly acquire aberrancies in energy metabolism and cellular redox state (Cairns et al., 2011).”
- Fatty acid uptake and lipid storage induced by HIF-1α contribute to cell growth and survival after hypoxia-reoxygenation. (2014, background): “Both of these processes promote rapid tumor cell growth (Cairns et al., 2011).”