ReviewMedical molecular morphology2018
Association between mutant IDHs and tumorigenesis in gliomas.
Review in Medical molecular morphology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting distinct amino acid metabolic vulnerabilities in IDH-mutant and IDH-wildtype gliomas.Acta neuropathologica communications · 2025Article
- The Role of Glia Telomere Dysfunction in the Pathogenesis of Central Nervous System Diseases.Molecular neurobiology · 2024Review
- A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024Review
- Glutathione promotes the synergistic effects of venetoclax and azacytidine against myelodysplastic syndrome‑refractory anemia by regulating the cell cycle.Experimental and therapeutic medicine · 2023Article
- Molecular and Circulating Biomarkers in Patients with Glioblastoma.International journal of molecular sciences · 2022Review
- A Genome-Wide Profiling of Glioma Patients with an IDH1 Mutation Using the Catalogue of Somatic Mutations in Cancer Database.Cancers · 2021Article
- Interrogation ofCancers · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To become immortalized, cells need to maintain the telomere length via the activation of telomerase or alternative lengthening of telomere. Mutations in IDH1/2 are strongly associated with the early stage of gliomagenesis. Previous work has shown that the accumulation of 2-HG, which is induced by mutant IDH1/2, inhibits α-KG-dependent deoxygenase and leads to genome-wide histone and DNA methylation alterations. These alterations are believed to contribute to tumorigenesis. H-Ras can transform human astrocytes with the inactivation of p53/pRb and expression of hTERT; however, mutant IDH1 can also transform cells. Moreover, mutant IDH1 can drive the immortalization and transformation of p53-/pRb-deficient astrocytes by reactivating telomerase and stabilizing telomeres in combination with increased histone lysine methylation and c-Myc/Max binding at the TERT promoter. It remains unclear whether mutant IDH1/2 acts only as the initial driver of gliomagenesis or it maintains transformed cells. Clinical studies are being performed to assess the use of mutant IDH1/2 inhibitors for treating gliomas.
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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.