ReviewCancers2018
Beyond Brooding on Oncometabolic Havoc in IDH-Mutant Gliomas and AML: Current and Future Therapeutic Strategies.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 41 citations in OpenAlex.
- TET2-driven demethylation of ANG promotes angiogenesis and malignant transformation in oligodendroglioma.Oncogene · 2026Article
- Outcome of Acute Myeloid Leukemia Treatment and Isocitrate Dehydrogenase (IDH) Mutations: A Systematic Review and Meta-Analysis Study.International journal of hematology-oncology and stem cell research · 2026Review
- Mechanism analysis and targeted therapy of IDH gene mutation in glioma.American journal of cancer research · 2025Review
- Tricarboxylic Acid Cycle Relationships with Non-Metabolic Processes: A Short Story with DNA Repair and Its Consequences on Cancer Therapy Resistance.International journal of molecular sciences · 2024Review
- Metabolo-epigenetic interplay provides targeted nutritional interventions in chronic diseases and ageing.Frontiers in oncology · 2023Review
- Article
- Advanced multiparametric MRI-based scoring for isocitrate dehydrogenase mutation prediction of gliomas.Polish journal of radiology · 2022Article
- Recent advances of IDH1 mutant inhibitor in cancer therapy.Frontiers in pharmacology · 2022Review
- Proteomics-based prognostic signature and nomogram construction of hypoxia microenvironment on deteriorating glioblastoma (GBM) pathogenesis.Scientific reports · 2021Article
- IDH Inhibitors and Beyond: The Cornerstone of Targeted Glioma Treatment.Molecular diagnosis & therapy · 2021Review
- Association of Circadian Clock Gene Expression with Glioma Tumor Microenvironment and Patient Survival.Cancers · 2021Article
- Genomic Space ofInternational journal of molecular sciences · 2021Article
- IDH mutation in glioma: molecular mechanisms and potential therapeutic targets.British journal of cancer · 2020Review
- Review
- To be Wild or Mutant: Role of Isocitrate Dehydrogenase 1 (IDH1) and 2-Hydroxy Glutarate (2-HG) in Gliomagenesis and Treatment Outcome in Glioma.Cellular and molecular neurobiology · 2020Review
- The Value of Enhanced MR Radiomics in Estimating the IDH1 Genotype in High-Grade Gliomas.BioMed research international · 2020Article
- Novel approaches for glioblastoma treatment: Focus on tumor heterogeneity, treatment resistance, and computational tools.Cancer reports (Hoboken, N.J.) · 2019Article
- Epigenetic Reprogramming for TargetingCancers · 2019Review
- Consequences ofMolecules (Basel, Switzerland) · 2019Review
- Mutant Isocitrate Dehydrogenase Inhibitors as Targeted Cancer Therapeutics.Frontiers in oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isocitrate dehydrogenases 1 and 2 (IDH1,2), the key Krebs cycle enzymes that generate NADPH reducing equivalents, undergo heterozygous mutations in >70% of low- to mid-grade gliomas and ~20% of acute myeloid leukemias (AMLs) and gain an unusual new activity of reducing the α-ketoglutarate (α-KG) to D-2 hydroxyglutarate (D-2HG) in a NADPH-consuming reaction. The oncometabolite D-2HG, which accumulates >35 mM, is widely accepted to drive a progressive oncogenesis besides exacerbating the already increased oxidative stress in these cancers. More importantly, D-2HG competes with α-KG and inhibits a large number of α-KG-dependent dioxygenases such as TET (Ten-eleven translocation), JmjC domain-containing KDMs (histone lysine demethylases), and the ALKBH DNA repair proteins that ultimately lead to hypermethylation of the CpG islands in the genome. The resulting CpG Island Methylator Phenotype (CIMP) accounts for major gene expression changes including the silencing of the MGMT (
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Identifiers
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.