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Citations to this article

Exploiting tumor metabolism: challenges for clinical translation
Matthew G. Vander Heiden
Matthew G. Vander Heiden
Published September 3, 2013
Citation Information: J Clin Invest. 2013;123(9):3648-3651. https://doi.org/10.1172/JCI72391.
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Review Series Article has an altmetric score of 9

Exploiting tumor metabolism: challenges for clinical translation

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Abstract

The metabolism of cancer cells differs from most normal cells, but how to exploit this difference for patient benefit is incompletely understood. Cancer cells require altered metabolism to efficiently incorporate nutrients into biomass and support abnormal proliferation. In addition, the survival of tumor cells outside of a normal tissue context requires adaptation of metabolism to different microenvironments. Some existing chemotherapies target metabolic enzymes, and there is a resurgent interest in developing new cancer drugs that interfere with metabolism. Success with this approach depends on understanding why specific metabolic pathways are important for cancer cells, determining how best to select patients, and developing technologies for monitoring patient response to therapies that target metabolic enzymes. The articles in this Review series address these issues, with a focus on how altered metabolism might influence tumor progression and how this knowledge might inform the use of new therapies targeting cancer metabolism. Emerging biomarker strategies to guide drug development are also highlighted.

Authors

Matthew G. Vander Heiden

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Total citations by year

Year: 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 Total
Citations: 2 1 1 2 4 1 6 5 5 8 10 45
Citation information
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Citations to this article (45)

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Specific changes in amino acid profiles in monocytes of patients with breast, lung, colorectal and ovarian cancers.
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Frontiers in immunology 2024
Critical roles and clinical perspectives of RNA methylation in cancer
Li G, Yao Q, Liu P, Zhang H, Liu Y, Li S, Shi Y, Li Z, Zhu W
2024
Compensatory cross-talk between autophagy and glycolysis regulates senescence and stemness in heterogeneous glioblastoma tumor subpopulations.
Martell E, Kuzmychova H, Senthil H, Kaul E, Chokshi CR, Venugopal C, Anderson CM, Singh SK, Sharif T
Acta Neuropathologica Communications 2023
Mitochondrial metabolic determinants of multiple myeloma growth, survival, and therapy efficacy
Nair R, Gupta P, Shanmugam M
Frontiers in Oncology 2022
Vascular Normalization: A New Window Opened for Cancer Therapies
T Yang, H Xiao, X Liu, Z Wang, Q Zhang, N Wei, X Guo
Frontiers in Oncology 2021
The metabolic landscape of RAS-driven cancers from biology to therapy
S Mukhopadhyay, MG Heiden, F McCormick
2021
Epigenetic CRISPR screens identify Npm1 as a therapeutic vulnerability in non-small cell lung cancer
F Li, WL Ng, TA Luster, H Hu, VO Sviderskiy, CM Dowling, KE Hollinshead, P Zouitine, H Zhang, Q Huang, M Ranieri, W Wang, Z Fang, T Chen, J Deng, K Zhao, HC So, A Khodadadi-Jamayran, M Xu, A Karatza, V Pyon, S Li, Y Pan, K Labbe, C Almonte, JT Poirier, G Miller, R Possemato, J Qi, KK Wong
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Low glucose induces mitochondrial reactive oxygen species via fatty acid oxidation in bovine aortic endothelial cells
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S Bernhardt, M Bayerlová, M Vetter, A Wachter, D Mitra, V Hanf, T Lantzsch, C Uleer, S Peschel, J John, J Buchmann, E Weigert, KF Bürrig, C Thomssen, U Korf, T Beissbarth, S Wiemann, EJ Kantelhardt
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