ArticleNeuro-oncology2022
The intrinsic and microenvironmental features of diffuse midline glioma: Implications for the development of effective immunotherapeutic treatment strategies.
Article in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Machine learning in neuroimaging for predicting H3K27M mutations in diffuse midline gliomas: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- Pilot report of an anti-PD-1/VEGF bispecific antibody for treating recurrent H3K27M-mutant diffuse midline gliomas.Cancer immunology, immunotherapy : CII · 2026Article
- Clinical, surgical, and molecular characteristics and outcomes of adult patients with diffuse midline glioma, H3 K27-altered, treated with surgical resection.Journal of neuro-oncology · 2026Article
- Myeloid compartment reprogramming through nanoparticle-delivered resiquimod blocks paracrine growth support and activates phagocytosis to slow tumor progression in endogenous mouse medulloblastoma and diffuse midline glioma models.bioRxiv : the preprint server for biology · 2026Article
- Ultrasound-Enhanced Drug Delivery in Pediatric Neuro-Oncology: A New Therapeutic Strategy.Pharmaceutics · 2026Review
- Preclinical efficacy of combinatorial B7-H3 CAR T cells and ONC206 against diffuse intrinsic pontine glioma.Neuro-oncology · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Diffuse Midline Gliomas: Clinical, Diagnostic, and Therapeutic Perspectives.Biomedicines · 2026Review
- Deciphering the tumor microenvironment and role of immunotherapy in diffuse midline glioma: A scoping review.Neuro-oncology · 2026Article
- Consequences of irradiation on blood-brain tumor barrier model of Diffuse Midline Glioma: characterization of physical and metabolic properties.Fluids and barriers of the CNS · 2026Article
- Radiotherapy plus neoadjuvant and concomitant IL-13Rα2-directed immunotoxin therapy for diffuse intrinsic pontine glioma.Communications biology · 2026Article
- Immune infiltration differences underlying prognostic radiomics subtypes from matched MRI and RNA sequencing in patients with lower-grade gliomas.Discover oncology · 2026Article
- Vaccine therapy for pediatric high-grade glioma: current landscape, challenges, and future directions.Journal of neuro-oncology · 2026Review
- Reprogramming tumor-associated macrophages in DMG/DIPG: emerging molecular and biophysical strategies.Frontiers in immunology · 2026Review
- Beyond base camp: PI3K/mTOR inhibition for the treatment of pediatric high-grade gliomas.Neuro-oncology · 2025Review
- BEHAV3D Tumor Profiler to map heterogeneous cancer cell behavior in the tumor microenvironment.eLife · 2025Article
- Comprehensive analysis of immune escape-related prognostic signature in high-grade glioma.Discover oncology · 2025Article
- Co-detection of mutations and methylations in cerebrospinal fluid ctdna for minimally-invasive diagnosis of brainstem glioma.Journal of experimental & clinical cancer research : CR · 2025Article
- H3K27M diffuse midline glioma is homologous recombination defective and sensitized to radiotherapy and NK cell-mediated antitumor immunity by PARP inhibition.Neuro-oncology · 2025Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse midline glioma (DMG), including those of the brainstem (diffuse intrinsic pontine glioma), are pediatric tumors of the central nervous system (CNS). Recognized as the most lethal of all childhood cancers, palliative radiotherapy remains the only proven treatment option, however, even for those that respond, survival is only temporarily extended. DMG harbor an immunologically "cold" tumor microenvironment (TME) with few infiltrating immune cells. The mechanisms underpinning the cold TME are not well understood. Low expression levels of immune checkpoint proteins, including PD-1, PD-L1, and CTLA-4, are recurring features of DMG and likely contribute to the lack of response to immune checkpoint inhibitors (ICIs). The unique epigenetic signatures (including stem cell-like methylation patterns), a low tumor mutational burden, and recurring somatic mutations (H3K27M, TP53, ACVR1, MYC, and PIK3CA), possibly play a role in the reduced efficacy of traditional immunotherapies. Therefore, to circumvent the lack of efficacy thus far seen for the use of ICIs, adoptive cell transfer (including chimeric antigen receptor T cells) and the use of oncolytic viruses, are currently being evaluated for the treatment of DMG. It remains an absolute imperative that we improve our understanding of DMG's intrinsic and TME features if patients are to realize the potential benefits offered by these sophisticated treatments. Herein, we summarize the limitations of immunotherapeutic approaches, highlight the emerging safety and clinical efficacy shown for sophisticated cell-based therapies, as well as the evolving knowledge underpinning the DMG-immune axis, to guide the development of immunotherapies that we hope will improve outcomes.
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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.