ReviewJournal of blood medicine2016
IDH1 and IDH2 mutations as novel therapeutic targets: current perspectives.
Review in Journal of blood medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 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
121 citing papers in PubMed, 215 citations in OpenAlex.
- Olutasidenib demonstrates significant clinical activity in mutated IDH1 acute myeloid leukaemia arising from a prior myeloproliferative neoplasm.British journal of haematology · 2025Trial
- Increased glioblastoma risk in patients with myeloproliferative neoplasms and myelodysplastic syndromes.Clinical and experimental medicine · 2026Article
- Clinicopathologic features of KRAS G12C-mutated non-small cell lung carcinomas:insights from 279 retrospective cases.Virchows Archiv : an international journal of pathology · 2026Article
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- A targeted metabolomic method to detect epigenetically relevant metabolites.Molecular metabolism · 2026Article
- TNMR in biomedicine · 2026Article
- Mechanisms of Metabolic Reprogramming Regulating Immunosuppression in the Gastric Cancer Tumor Microenvironment.Biomolecules · 2026Review
- Current Pharmacotherapeutic Strategies in Diffuse Gliomas: Focus on Glioblastoma, IDH-Wildtype, and Emerging Targeted Therapies for IDH-Mutant Tumors.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Research on Targeted Therapy for Malignant Tumors of the Biliary Tract.OncoTargets and therapy · 2026Review
- Article
- Article
- Machine learning-based identification of exosome-related biomarkers and drugs prediction in nasopharyngeal carcinoma.Discover oncology · 2025Article
- Genomic landscape of biliary tract cancer and corresponding targeted treatment strategies.International journal of clinical oncology · 2025Review
- Nanotechnology in brain cancer treatment: The role of gold nanoparticles as therapeutic enhancers.Ibrain · 2025Review
- Review
- 3D-QSAR, Scaffold Hopping, Virtual Screening, and Molecular Dynamics Simulations of Pyridin-2-one as mIDH1 Inhibitors.International journal of molecular sciences · 2024Article
- Molecular Targeting of the Isocitrate Dehydrogenase Pathway and the Implications for Cancer Therapy.International journal of molecular sciences · 2024Review
- Methylation-Based Characterization of a NewInternational journal of molecular sciences · 2024Article
- Identification of ALDOB as a novel prognostic biomarker in kidney clear cell renal cell carcinoma.Heliyon · 2024Article
- The clinical regimens and cell membrane camouflaged nanodrug delivery systems in hematologic malignancies treatment.Frontiers in pharmacology · 2024Review
61 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
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are key metabolic enzymes that convert isocitrate to α-ketoglutarate. IDH1/2 mutations define distinct subsets of cancers, including low-grade gliomas and secondary glioblastomas, chondrosarcomas, intrahepatic cholangiocarcinomas, and hematologic malignancies. Somatic point mutations in IDH1/2 confer a gain-of-function in cancer cells, resulting in the accumulation and secretion in vast excess of an oncometabolite, the D-2-hydroxyglutarate (D-2HG). Overproduction of D-2HG interferes with cellular metabolism and epigenetic regulation, contributing to oncogenesis. Indeed, high levels of D-2HG inhibit α-ketoglutarate-dependent dioxygenases, including histone and DNA demethylases, leading to histone and DNA hypermethylation and finally a block in cell differentiation. Furthermore, D-2HG is a biomarker suitable for the detection of IDH1/2 mutations at diagnosis and predictive of the clinical response. Finally, mutant-IDH1/2 enzymes inhibitors have entered clinical trials for patients with IDH1/2 mutations and represent a novel drug class for targeted therapy.
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.