ReviewCell & bioscience2017
Isocitrate dehydrogenases in physiology and cancer: biochemical and molecular insight.
Review in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 119 citations in OpenAlex.
- Revisiting retinoic acid in AML therapy: mechanisms of action and rational combination strategies.British journal of cancer · 2026Review
- Nuclear IDH3A Drives Transcriptional Programs in Melanoma via the YBX1-JUN/FOS Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- State of the Art of IDH Inhibitors: Emerging Questions and Perspectives.Anti-cancer agents in medicinal chemistry · 2026Review
- 2-Hydroxyglutarate in onco-pathway: a metabolic driver of proto-oncogene activation.Frontiers in oncology · 2026Review
- Integrative machine learning-guidedRSC advances · 2025Article
- Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) represses sulfide:quinone oxidoreductase expression and targets the sulfido-redox system in glioblastoma models.Redox report : communications in free radical research · 2025Article
- Review
- Modeling the metabolic response of A2780 ovarian cancer cells to gold-based cytotoxic drugs.NPJ systems biology and applications · 2025Article
- Article
- In defence of ferroptosis.Signal transduction and targeted therapy · 2025Review
- NADPCurrent medicinal chemistry · 2025Review
- Prokaryotic organelle mitochondria drive tumorigenesis: "the original sin".Frontiers in oncology · 2025Review
- Neomorphic IDH Heterodimer Mutants: An Underestimated Point in Cancer Pathogenesis.Current cancer drug targets · 2025Review
- IDH2 and GLUD1 depletion arrests embryonic development through an H4K20me3 epigenetic barrier in porcine parthenogenetic embryos.Zoological research · 2024Article
- Proteo-metabolomics and patient tumor slice experiments point to amino acid centrality for rewired mitochondria in fibrolamellar carcinoma.Cell reports. Medicine · 2024Article
- Energy metabolism-related GLUD1 contributes to favorable clinical outcomes of IDH-mutant glioma.BMC neurology · 2024Article
- Homeostatic regulation of NAD(H) and NADP(H) in cells.Genes & diseases · 2024Review
- Analysis of IDH and EGFR as biomarkers in glioblastoma multiforme: A case-control study.Heliyon · 2024Article
- Clinical Implications of Isocitrate Dehydrogenase Mutations and Targeted Treatment of Acute Myeloid Leukemia with Mutant Isocitrate Dehydrogenase Inhibitors-Recent Advances, Challenges and Future Prospects.International journal of molecular sciences · 2024Review
9 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isocitrate dehydrogenases play important roles in cellular metabolism and cancer. This review will discuss how the roles of isoforms 1 and 2 in normal cell and cancer metabolism are distinct from those of isoform 3. It will also explain why, unlike 1 and 2, mutations in isoform 3 in tumor are not likely to be driver ones. A model explaining two important features of isocitrate dehydrogenases 1 and 2 mutations, their dominant negative effect and their mutual exclusivity, will be provided. The importance of targeting these mutations and the possibility of augmenting such therapy by targeting other cancer-related pathways will also be discussed.
Indexed as
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.