ArticleNature metabolism2020
An enolase inhibitor for the targeted treatment of ENO1-deleted cancers.
Article in Nature metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 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
57 citing papers in PubMed, 98 citations in OpenAlex.
- ENO1 promotes acute myeloid leukemia progression through SCD1-mediated lipid metabolism reprogramming.Blood advances · 2026Article
- Targeting enolase isoenzyme 2 enables precision glycolysis inhibition in VHL-mutant renal cell carcinoma.Cell death & disease · 2026Article
- ENO2 sustains cancer stemness and metastatic competence through a phosphoenolpyruvate-dependent metabolic axis in triple-negative breast cancer.Cell death & disease · 2026Article
- 1p/19q codeletion induces targetable and imageable vulnerabilities in glucose metabolism in oligodendrogliomas.Neuro-oncology · 2026Article
- Context-dependent synthetic lethality - an emerging precision therapeutic approach.Nature reviews. Cancer · 2026Review
- HIF-1α Promotes Macrophage Extracellular Trap Formation and Exacerbates Acute Lung Injury in Neonatal Sepsis.Biomedicines · 2026Article
- H4K5 lactylation - ENO2 loop drives glycolysis and HCC progression.JHEP reports : innovation in hepatology · 2026Article
- Enolase 1: A paradigm of metabolic enzyme moonlighting in tumorigenesis (Review).International journal of oncology · 2026Review
- Review
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- Glycolysis and glycolytic enzymes in acute myeloid leukemia: Warburg and beyond.Frontiers in pharmacology · 2026Review
- Drug Repurposing in Glioblastoma Using a Machine Learning-Based Hybrid Feature Selection Approach.International journal of molecular sciences · 2025Article
- Targeted Metabolomic Methods forJournal of proteome research · 2025Article
- Recent advances in natural and synthetic phosphonate therapeutics.Current opinion in microbiology · 2025Review
- The Landscape of Cancer Metabolism as a Therapeutic Target.Pathology international · 2025Review
- Glucose metabolism and its direct action in cancer and immune regulation: opportunities and challenges for metabolic targeting.Journal of biomedical science · 2025Review
- Integrative Single-Cell and Bulk RNA Sequencing Identifies a Glycolysis-Related Prognostic Signature for Predicting Prognosis in Pancreatic Cancer.International journal of molecular sciences · 2025Article
- Dynamic investigation of hypoxia-induced L-lactylation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Towards next-generation treatment options to combat Plasmodium falciparum malaria.Nature reviews. Microbiology · 2025Review
- Targeting Malaria's Achilles' Heels: A Review of Plasmodium Life Cycle Vulnerabilities for Drug Discovery.Current topics in medicinal chemistry · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
31 authors at 2 institutions in 1 country.
Funding
Abstract
Inhibiting glycolysis remains an aspirational approach for the treatment of cancer. We have previously identified a subset of cancers harbouring homozygous deletion of the glycolytic enzyme enolase (ENO1) that have exceptional sensitivity to inhibition of its redundant paralogue, ENO2, through a therapeutic strategy known as collateral lethality. Here, we show that a small-molecule enolase inhibitor, POMHEX, can selectively kill ENO1-deleted glioma cells at low-nanomolar concentrations and eradicate intracranial orthotopic ENO1-deleted tumours in mice at doses well-tolerated in non-human primates. Our data provide an in vivo proof of principle of the power of collateral lethality in precision oncology and demonstrate the utility of POMHEX for glycolysis inhibition with potential use across a range of therapeutic settings.
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What OpenQuestion holds
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.