Cancer Cell Metabolism: One Hallmark, Many Faces
By J. Cantor, David M. Sabatini. Cancer Discovery, 2012
892 citations recorded by the source corpus.
Cancer cells must rewire cellular metabolism to satisfy the demands of growth and proliferation. While many of the metabolic alterations are largely similar to those in normal proliferating cells, they are aberrantly driven in cancer by a combination of genetic lesions and non-genetic factors such as the tumor microenvironment. However, a single model of altered tumor metabolism does not describe the sum of metabolic changes that can support cell growth. Instead, the diversity of such changes within the metabolic program of a cancer cell can dictate by what means proliferative rewiring is driven, and can also impart heterogeneity in the metabolic dependencies of the cell. A better understanding of this heterogeneity may enable the development and optimization of therapeutic strategies that target tumor metabolism.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0805929668a504a0ced6c260aeaa6a5c8692f245
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In Cancer Research
- P. Vaupel
- Gabriele Multhoff
- Ajla T. Wasti
- Ralph J. Deberardinis
- C. Hensley
- Navdeep S. Chandel
- A. Mayer
- M. V. Vander Heiden
In Molecular Biology
- P. Vaupel
- Ajla T. Wasti
- Gabriele Multhoff
- Ralph J. Deberardinis
- C. Hensley
- M. V. Vander Heiden
- C. V. Dang
Citations in the corpus
- The lipid kinase PI5P4Kβ is an intracellular GTP sensor for metabolism and tumorigenesis (2016, neutral): “Mo their metabolism in order to cope with nutrient and energy stresses during tumorigenesis (Cantor and Sabatini, 2012; Jones and Thompson, 2009; Laderoute et al., 2006; Schafer et al., 2009).”
- Glutamine oxidation maintains the TCA cycle and cell survival during impaired mitochondrial pyruvate transport (2014, background): “In mammals, glucose and glutamine are two of the most abundant nutrients to support these functions (Cantor and Sabatini, 2012).”
- Revisiting the Warburg effect: historical dogma versus current understanding (2020, background): “…(h) interactions with the hostile TME and cancer-associated stromal cells, and (i) maintenance of the pHi–pHe gradient (Semenza, 2010; Cantor & Sabatini, 2012; Martinez-Pastor & Mostolavsky, 2012; Faubert et al. 2013; Lu et al. 2015; Tran et al. 2016; He et al. 2017; Yu et al.…”