ReviewOncogene2020
Endogenous toxic metabolites and implications in cancer therapy.
Review in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- Self-assembled metabolite-derived amyloid-like structures: implications for disease, therapeutics, and biomedical applications.Molecular biology reports · 2026Review
- Article
- Biomedical Applications of Nanozymes: An Enzymology Perspective.Angewandte Chemie (International ed. in English) · 2025Review
- Toxic aldehydes in cooking vegetable oils: Generation, toxicity and disposal methods.Food chemistry: X · 2025Review
- TgGloL is an atypical glyoxalase/VOC domain-containing apicoplast protein that is important for the growth ofMolecular biology of the cell · 2025Article
- Polymeric nanocarriers for therapeutic gene delivery.Asian journal of pharmaceutical sciences · 2025Review
- Machine Learning in Early Prediction of Metabolism of Drugs.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025Review
- Unveiling Colorectal Cancer Biomarkers: Harnessing Biosensor Technology for Volatile Organic Compound Detection.Sensors (Basel, Switzerland) · 2024Review
- Article
- Kinome-Wide Synthetic Lethal Screen Identifies PANK4 as a Modulator of Temozolomide Resistance in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Discretised Flux Balance Analysis for Reaction-Diffusion Simulation of Single-Cell Metabolism.Bulletin of mathematical biology · 2024Article
- Immunomodulatory effects of cysteamine and its potential use as a host-directed therapy for tuberculosis.Frontiers in immunology · 2024Article
- The Development of Organotin(IV) N-Ethyl-N-Benzyldithiocarbamate Complexes: A Study on Their Synthesis, Characterization, and Cytocidal Effects on A549 Cell Line.Anti-cancer agents in medicinal chemistry · 2024Article
- Lethal metabolism of Candida albicans respiratory mutants.PloS one · 2024Article
- Disruption of sugar nucleotide clearance is a therapeutic vulnerability of cancer cells.Nature · 2023Article
- Natural compounds targeting nuclear receptors for effective cancer therapy.Cancer metastasis reviews · 2023Review
- Cell-Penetrating Peptide-Based Delivery of Macromolecular Drugs: Development, Strategies, and Progress.Biomedicines · 2023Review
- Cultured Meat Safety Research Priorities: Regulatory and Governmental Perspectives.Foods (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well recognized that many metabolic enzymes play essential roles in cancer cells in producing building blocks such as nucleotides, which are required in greater amounts due to their increased proliferation. On the other hand, the significance of enzymes in preventing the accumulation of their substrates is less recognized. Here, we outline the evidence and underlying mechanisms for how many metabolites normally produced in cells are highly toxic, such as metabolites containing reactive groups (e.g., methylglyoxal, 4-hydroxynonenal, and glutaconyl-CoA), or metabolites that act as competitive analogs against other metabolites (e.g., deoxyuridine triphosphate and l-2-hydroxyglutarate). Thus, if a metabolic pathway contains a toxic intermediate, then we may be able to induce accumulation and poison a cancer cell by targeting the downstream enzyme. Furthermore, this poisoning may be cancer cell selective if this pathway is overactive in a cancer cell relative to a nontransformed cell. We describe this concept as illustrated in selenocysteine metabolism and other pathways and discuss future directions in exploiting toxic metabolites to kill cancer cells.
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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.