ReviewGenes & diseases2020
Metabolic reprogramming in tumors: Contributions of the tumor microenvironment.
Review in Genes & diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 90 citations in OpenAlex.
- Integrated single-cell and spatial transcriptomic analyses reveal malignant epithelial glycolytic heterogeneity and spatial niche remodeling during colorectal cancer progression.Functional & integrative genomics · 2026Article
- Mechanism of ECM Stiffness-Integrin-Hippo-ABCG1 axis in regulating ferroptosis and targeted nanodrug intervention in LUAD.Respiratory research · 2025Article
- Cervical cancer molecular subtype identification and prognosis classification by a metabolism-related gene expression.Translational cancer research · 2025Article
- The integration of single-cell and metabolomics reveals the increase of oxidative phosphorylation during the liver metastasis of colorectal cancer.Cancer & metabolism · 2025Article
- Integrating Metabolic Modulation and Nanomedicine for Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Metabolomic Profiling Reveals Distinct Signatures in Primary and Secondary Polycythemia.Metabolites · 2025Article
- Metabolic landscape of clear cell renal cell carcinoma and search for metabolites predictive of drug response.BMC cancer · 2025Article
- Pan-cancer analysis of UDP-glucose 6-dehydrogenase in human tumors and its function in hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- Downregulation of UDP-glucose 6-dehydrogenase predicts adverse outcomes in patients with colorectal cancer and promotes tumorigenesis.Scientific reports · 2025Article
- Reprogrammed immuno-metabolic environment of cancer: the driving force of ferroptosis resistance.Molecular cancer · 2025Review
- Article
- Redox-responsive metal-organic framework nanocapsules enhance tumor chemo-immunotherapy by modulating tumor metabolic reprogramming.Materials today. Bio · 2025Article
- Triptolide reverses cis‑diamminedichloroplatinum resistance in esophageal squamous cell carcinoma by suppressing glycolysis and causing mitochondrial malfunction.Molecular medicine reports · 2025Article
- Bibliometric analysis of glycolysis and prostate cancer research from 2004 to 2024.Discover oncology · 2025Article
- Epigenetic and metabolic reprogramming via nanotechnology: a synergistic approach to cancer vaccination in lung tumors.Frontiers in genetics · 2025Review
- NMR-Based Stable Isotope Tracing of Cancer Metabolism.Methods in molecular biology (Clifton, N.J.) · 2025Article
- GNG7 as a tumor-suppressor gene in lung adenocarcinoma: implications for prognosis and immune-based therapies.Frontiers in oncology · 2025Article
- Approaches to investigate tissue-resident innate lymphocytes metabolism at the single-cell level.Nature communications · 2024Review
- Targeting PGK1: A New Frontier in Breast Cancer Therapy Under Hypoxic Conditions.Current issues in molecular biology · 2024Review
- Stable isotope-resolved metabolomics analyses of metabolic phenotypes reveal variable glutamine metabolism in different patient-derived models of non-small cell lung cancer from a single patient.Metabolomics : Official journal of the Metabolomic Society · 2024Article
4 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The genetic alterations associated with cell transformation are in large measure expressed in the metabolic phenotype as cancer cells proliferate and change their local environment, and prepare for metastasis. Qualitatively, the fundamental biochemistry of cancer cells is generally the same as in the untransformed cells, but the cancer cells produce a local environment, the TME, that is hostile to the stromal cells, and compete for nutrients. In order to proliferate, cells need sufficient nutrients, either those that cannot be made by the cells themselves, or must be made from simpler precursors. However, in solid tumors, the nutrient supply is often limiting given the potential for rapid proliferation, and the poor quality of the vasculature. Thus, cancer cells may employ a variety of strategies to obtain nutrients for survival, growth and metastasis. Although much has been learned using established cell lines in standard culture conditions, it is becoming clear from in vivo metabolic studies that this can also be misleading, and which nutrients are used for energy production versus building blocks for synthesis of macromolecules can vary greatly from tumor to tumor, and even within the same tumor. Here we review the operation of metabolic networks, and how recent understanding of nutrient supply in the TME and utilization are being revealed using stable isotope tracers in vivo as well as in vitro.
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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.