Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy?
By N. Hay. Nature Reviews. Cancer, 2016
998 citations recorded by the source corpus.
In recent years there has been a growing interest among cancer biologists in cancer metabolism. This Review summarizes past and recent advances in our understanding of the reprogramming of glucose metabolism in cancer cells, which is mediated by oncogenic drivers and by the undifferentiated character of cancer cells. The reprogrammed glucose metabolism in cancer cells is required to fulfil anabolic demands. This Review discusses the possibility of exploiting the reprogrammed glucose metabolism for therapeutic approaches that selectively target cancer cells.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b013339f8372bac6fe3102a18dd3d09b1fe6fdee
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In Cancer Research
In Molecular Biology
- D. Y. Gui
- Alba Luengo
- P. Vaupel
- M. V. Vander Heiden
- Gabriele Multhoff
- Y. Fouad
- C. Aanei
- Ralph J. Deberardinis
Citations in the corpus
- Revisiting the Warburg effect: historical dogma versus current understanding (2020, background): “DOI: 10.1113/JP278810 This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. essential part of a ‘s”
- Drug resistance and combating drug resistance in cancer (2019, background): “For example, it is well known from PET-scans that aggressive tumors with poor prognosis are almost always glucose/energy metabolism active tumors([203,204]).”
- Targeting Metabolism for Cancer Therapy (2017, background): “Substantial work has sought to target increased glycolysis including efforts to inhibit lactate production and excretion (Doherty and Cleveland, 2013; Hamanaka and Chandel, 2012; Hay, 2016; Pelicano et al., 2006; Zhao et al., 2013).”
- Revisiting the hallmarks of cancer. (2017, positive): “While an initial explanation to the phenomenon was defective oxidative phosphorylation [148], it is now established that cancer cells (generally) have normally-functioning mitochondria capable of oxidative phosphorylation; in fact targeting mitochondrial DNA reduces tumorigenic potential of cells bo”