Cited by 2,337Cancer, Hypoxia, and MetabolismMetabolism, Diabetes, and CancerCancer and biochemical research

Tumor cell metabolism: cancer's Achilles' heel

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Kroemer, Guido, Pouyssegur, Jacques·2008·Cancer Cell

Abstract

The essential hallmarks of cancer are intertwined with an altered cancer cell-intrinsic metabolism, either as a consequence or as a cause. As an example, the resistance of cancer mitochondria against apoptosis-associated permeabilization and the altered contribution of these organelles to metabolism are closely related. Similarly, the constitutive activation of signaling cascades that stimulate cell growth has a profound impact on anabolic metabolism. Here, we review the peculiarities of tumor cell metabolism that might be taken advantage of for cancer treatment. Specifically, we discuss the alterations in signal transduction pathways and/or enzymatic machineries that account for metabolic reprogramming of transformed cells.

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Crossref · 10.1016/j.ccr.2008.05.005

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Authors
Kroemer, G., & Pouyssegur, J.
Affiliations
Université Paris-Sud (FR)
Corresponding author
Kroemer, Guido
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2008-06
Volume
13
Issue
6
Pages
472-482
ISSN
1535-6108 (ISSN-L)
OpenAlex
W1991429659
Cited by
2,337
References
12
Citations by year
2026: 68 · 2025: 101 · 2024: 130 · 2023: 124 · 2022: 155 · 2021: 110 · 2020: 136 · 2019: 125 · 2018: 128 · 2017: 131 · 2016: 136 · 2015: 150 · 2014: 171 · 2013: 150 · 2012: 137
FWCI
9.18
Type
journal article
Language
en
Open access
Locations
  • Cancer Cell (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
Keywords
cancer metabolism, metabolic reprogramming, mitochondrial permeability transition, apoptosis resistance, signal transduction, anabolic metabolism, cancer therapy targets, cancer hallmarks
MeSH terms
Animals, Antineoplastic Agents, Energy Metabolism, Enzyme Inhibitors, Humans, Mitochondria, Neoplasm Invasiveness, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Drug Design, Signal Transduction, Apoptosis, Tumor Escape, Cell Proliferation

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