The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Cancer Cell Metabolism: One Hallmark, Many Faces
Open accessAbstract
Cancer cells must rewire cellular metabolism to satisfy the demands of growth and proliferation. Although 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 nongenetic 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. Significance: Altered tumor metabolism is now a generally regarded hallmark of cancer. Nevertheless, the recognition of metabolic heterogeneity in cancer is becoming clearer as a result of advancements in several tools used to interrogate metabolic rewiring and dependencies. Deciphering this context-dependent heterogeneity will supplement our current understanding of tumor metabolism and may yield promising therapeutic and diagnostic utilities. Cancer Discov; 2(10); 881–98. ©2012 AACR.
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Cites
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Regulation of cancer cell metabolism
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Cancer-associated IDH1 mutations produce 2-hydroxyglutarate
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Self-citationTSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
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Regulation of mammalian nucleotide metabolism and biosynthesis
Lane, A. N., & Fan, T. W.-M. (2015) · Nucleic Acids Research · doi:10.1093/nar/gkv047 · Cited by 959
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Vaupel, P., & Multhoff, G. (2021) · The Journal of Physiology · doi:10.1113/jp278810 · Cited by 830
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“The activated mTOR directly or indirectly stimulates metabolic reprogramming by activating key transcription factors, such as c-Myc, cyclin D, and hypoxia-inducible transcription factor 1 alpha (HIF-1α), even under normoxic conditions [32].”
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Metadata
- Authors
- Cantor, J. R., & Sabatini, D. M.
- Venue
- Cancer Discovery
- Published
- 2012-10-01
- Volume
- 2
- Issue
- 10
- Pages
- 881-898
- ISSN
- 2159-8274 (ISSN-L)
- 2159-8290
- OpenAlex
- W2118107482
- Cited by
- 947
- References
- 61
- FWCI
- 14.05
- Type
- journal article
- Language
- en
- Open access
- green
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