ReviewFrontiers in oncology2020
Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells.
Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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
30 citing papers in PubMed, 44 citations in OpenAlex.
- Gut microbiota metabolic reprogramming drives the development of metabolic diseases in the host.Gut microbes · 2026Review
- PhiKan 083 Inhibits MYCN Expression in Liver Cancer Cells Independent of p53 Pathways.ACS pharmacology & translational science · 2026Article
- 7,7"-dimethoxyagastisflavone induced MYCN/MYBL2-dependent apoptosis and metabolism reprogramming in Sonic Hedgehog medulloblastoma.Journal of translational medicine · 2026Article
- Predicting neuroblastoma prognosis using machine learning analysis of metabolism-related gene network perturbation.BMC pediatrics · 2026Article
- Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026Review
- Review
- The Warburg Effect and Aerobic Glycolysis in Tumors.Cancer treatment and research · 2026Review
- Integrative single-cell analysis revealsFrontiers in immunology · 2026Article
- Bidirectional crosstalk between ER stress and lipid metabolism: From proteostasis to tumor adaptation.Cell death discovery · 2025Review
- Noninvasive Prediction of Programmed Cell Death Protein-Ligand 1 Expression in Locally Advanced Non-small Cell Lung Cancer byAnnals of surgical oncology · 2025Article
- Lactylation-related gene signatures for prognosis and treatment response prediction in radiation-resistant non-small cell lung cancer.Discover oncology · 2025Article
- Cancer stem cells: landscape, challenges and emerging therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Mapping the landscape of metabolic reprogramming research in lung cancer: a bibliometric and visualized analysis.Discover oncology · 2025Article
- A high-throughput screening platform to identifyFrontiers in oncology · 2025Article
- Exploiting replication stress for synthetic lethality in MYC-driven cancers.American journal of cancer research · 2025Review
- The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.International journal of molecular sciences · 2024Review
- Article
- Prognostic analysis of E2F transcription factors E2F1 and E2F3 in four independent pediatric neuroblastoma cohorts.BMC pediatrics · 2022Article
- Drug resistance mechanisms create targetable proteostatic vulnerabilities in Her2+ breast cancers.PloS one · 2022Article
- Role of Energy Metabolism in the Progression of Neuroblastoma.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells generate large amounts of lactate derived from glucose regardless of the available oxygen level. Cancer cells finely control ATP synthesis by modulating the uptake of substrates and the activity of enzymes involved in aerobic glycolysis (Warburg effect), which enables them to adapt to the tumor microenvironment. However, increasing evidence suggests that mitochondrial metabolism, including the tricarboxylic acid (TCA) cycle, oxidative phosphorylation (OXPHOS), and glutaminolysis, is paradoxically activated in MYCN-amplified malignancies. Unlike non-amplified cells, MYCN-amplified cancer cells significantly promote OXPHOS-dependent ATP synthesis. Furthermore, tumor cells are differentially dependent on fatty acid β-oxidation (FAO) according to N-Myc status. Therefore, upregulation of FAO-associated enzymes is positively correlated with both N-Myc expression level and poor clinical outcome. This review explores therapeutic strategies targeting cancer stem-like cells for the treatment of tumors associated with MYCN amplification.
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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.