ReviewOncology reports2026
Epigenetic mechanisms and therapeutic advances in diffuse midline glioma (Review).
Review in Oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Diffuse Midline Gliomas: Clinical, Diagnostic, and Therapeutic Perspectives.Biomedicines · 2026Review
- Nanopore and EPIC array profiling unmask an atypical non-midline H3 K27-altered glioma: a case report.Frontiers in oncology · 2026Article
- Acetylation modification in malignant progression and therapeutic resistance of gliomas.Frontiers in cell and developmental biology · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gliomas are the most common primary malignant tumors of the central nervous system in adults, with diffuse midline gliomas (DMG) being particularly aggressive and associated with inferior survival rate. Notwithstanding advances in molecular diagnostics and epigenetics, the specific pathological mechanisms of DMG remain to be fully elucidated. A series of studies have demonstrated that histone modifications, particularly the histone H3 lysine 27 (H3K27)M mutation, play a pivotal role in the development and progression of DMG. The mutation disrupts histone methylation and acetylation to induce widespread gene expression abnormalities, tumor aggressiveness and treatment resistance. Conventional treatments such as surgery, local radiotherapy and chemotherapy offer limited efficacy. However, emerging precision therapies targeting histone mutations, epigenetic modifications and innovative immunotherapies show promise in improving outcomes. The present study provided a comprehensive overview of the molecular mechanisms, epigenetic characteristics and the latest therapeutic advances in DMG. By investigating the H3K27M mutation and its associated epigenetic mechanisms, the present review aimed to establish theoretical frameworks and research avenues for developing precise therapeutic strategies for DMG, thus contributing to advancing the field of personalized medicine.
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.