Metabolic targets for cancer therapy
By L. Galluzzi, Oliver Kepp, M. V. Vander Heiden, Guido Kroemer. Nature reviews. Drug discovery, 2013
641 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/3d182fde384b601c5437723ddf662ff82dc1ada7
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
- Guido Kroemer
- L. Galluzzi
- Alec C. Kimmelman
- Huafeng Zhang
- D. Y. Gui
- Zhaoyong Li
- Alba Luengo
- M. V. Vander Heiden
In Molecular Biology
- Guido Kroemer
- L. Galluzzi
- Beth Levine
- Douglas R. Green
- Seamus J. Martin
- Alec C. Kimmelman
- D. Rubinsztein
- Eric H. Baehrecke
Citations in the corpus
- Reprogramming of glucose, fatty acid and amino acid metabolism for cancer progression (2015, background): “Besides glycolytic rate-limiting enzymes, glucose transporters and other metabolic enzymes have also been selected as targets for drug screening [151].”
- Autophagy in malignant transformation and cancer progression (2015, positive): “…and antioxidant defenses, (2) mitochondrial respiration remains high to satisfy increased energy demands; and (3) several amino acids, including glutamine and serine, become essential as a means to cope with exacerbated metabolic functions (Hanahan & Weinberg, 2011; Galluzzi et al , 2013).”
- Mitochondrial metabolism and cancer (2017, background): “One of the main problems with targeting mitochondria as a strategy to kill malignant cells or sensitize them to treatment is that multiple immune effector cells, and in particular CD8 cytotoxic T lymphocytes (CTLs, which are involved in the efficacy of many – if not all – therapies), display remarka”
- Targeting Metabolism for Cancer Therapy (2017, background): “…the aberrant metabolism of proliferating cancer cells presents potential opportunities, and there has been a growing interest in studying how best to target cancer metabolism (Bobrovnikova-Marjon and Hurov, 2014; Galluzzi et al., 2013; MartinezOutschoorn et al., 2017; Vander Heiden, 2011).”
- Metabolic control of cell death (2014, background): “bisphosphatase) favors PMK2 inactivation (5).”