ReviewCancer biology & therapy2011
Tumor cell metabolism: an integral view.
Review in Cancer biology & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
122 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- A systematic review of metabolomic profiling of gastric cancer and esophageal cancer.Cancer biology & medicine · 2020Pooled it
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- Metabolomic Effects and Their Relationship with Intracellular/Extracellular Concentrations of CasiopeinasInternational journal of molecular sciences · 2025Article
- Exploring the Potential of Zein Nanoparticles in Personalised Cancer Therapy, Highlighting Their Various Methodologies, Applications and Challenges.Journal of cellular and molecular medicine · 2025Review
- Blood metabolites, mitochondrial biofunction, and cervical cancer: a bidirectional Mendelian randomization study.BMC women's health · 2025Article
- Identification of picornavirus proteins that inhibit de novo nucleotide synthesis during infection.PLoS pathogens · 2025Article
- Repurposing brucine as a chemopreventive agent in mammary gland carcinoma: Regulating lactate transport through MCT-4.Toxicology reports · 2025Article
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- "Effects of Redox Status on Immediate Hypericin-Mediated Photodynamic Therapy in Human Glioblastoma T98G Cell Line".ACS omega · 2025Article
- 2-Deoxy-D-Glucose and ES-936 sensitize cancer- but not normal cells to both low- and high LET irradiation.Frontiers in oncology · 2025Article
- From gut to proteomics: the impact ofFrontiers in oncology · 2025Article
- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
- Impact of oxytosis on the cross-talk of mTORC with mitochondrial proteins in drug-resistant cancer stem cells.Journal of cellular physiology · 2024Review
- Detection of the Fatty Acid Metabolism-Linked Genes in Lung Adenocarcinoma as Biomarkers for Clinical Prognosis and Immunotherapeutic Targets.The clinical respiratory journal · 2024Article
- lncRNAs as prognostic markers and therapeutic targets in cuproptosis-mediated cancer.Clinical and experimental medicine · 2024Review
- Veillonella parvula as an anaerobic lactate-fermenting bacterium for inhibition of tumor growth and metastasis through tumor-specific colonization and decrease of tumor's lactate level.Scientific reports · 2024Article
- Understanding the intersection between placental development and cancer: Lessons from the tumor suppressor BAP1.Communications biology · 2024Review
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is a genetic disease that is caused by mutations in oncogenes, tumor suppressor genes and stability genes. The fact that the metabolism of tumor cells is altered has been known for many years. However, the mechanisms and consequences of metabolic reprogramming have just begun to be understood. In this review, an integral view of tumor cell metabolism is presented, showing how metabolic pathways are reprogrammed to satisfy tumor cell proliferation and survival requirements. In tumor cells, glycolysis is strongly enhanced to fulfill the high ATP demands of these cells; glucose carbons are the main building blocks in fatty acid and nucleotide biosynthesis. Glutaminolysis is also increased to satisfy NADPH regeneration, whereas glutamine carbons replenish the Krebs cycle, which produces metabolites that are constantly used for macromolecular biosynthesis. A characteristic feature of the tumor microenvironment is acidosis, which results from the local increase in lactic acid production by tumor cells. This phenomenon is attributed to the carbons from glutamine and glucose, which are also used for lactic acid production. Lactic acidosis also directs the metabolic reprogramming of tumor cells and serves as an additional selective pressure. Finally, we also discuss the role of mitochondria in supporting tumor cell metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.