Evidence map›Paper›PMID 26034626›Full record

ArticleNeuro-oncology practice2014

Management of high-grade gliomas in the pediatric patient: Past, present, and future.

Magimairajan Issai Vanan, David D Eisenstat

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology practice, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Dabrafenib in pediatric patients withNeuro-oncology practice · 2025
    Article
  7. Review
  8. Bevacizumab in Pediatric Neuro-Oncology.Current oncology (Toronto, Ont.) · 2025
    Review
  9. Review
  10. Article
  11. Epigenetics to clinicopathological features: a bibliometric analysis of H3 G34-mutant diffuse hemispheric glioma literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Magimairajan Issai VananSection of Pediatric Hematology/Oncology/BMT, CancerCare Manitoba, Departments of Pediatrics & Child Health and Biochemistry & Medical Genetics , University of Manitoba , Winnipeg, Manitoba , Canada (M.I.V.); Division of Hematology/Oncology and Palliative Care, Stollery Children's Hospital, Departments of Pediatrics, Medical Genetics and Oncology , University of Alberta , Edmonton, Alberta , Canada (D.D.E.).
David D EisenstatSection of Pediatric Hematology/Oncology/BMT, CancerCare Manitoba, Departments of Pediatrics & Child Health and Biochemistry & Medical Genetics , University of Manitoba , Winnipeg, Manitoba , Canada (M.I.V.); Division of Hematology/Oncology and Palliative Care, Stollery Children's Hospital, Departments of Pediatrics, Medical Genetics and Oncology , University of Alberta , Edmonton, Alberta , Canada (D.D.E.).
Stollery Children's Hospital · CAUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-grade gliomas (HGGs) constitute ∼15% of all primary brain tumors in children and adolescents. Routine histopathological diagnosis is based on tissue obtained from biopsy or, preferably, from the resected tumor itself. The majority of pediatric HGGs are clinically and biologically distinct from histologically similar adult malignant gliomas; these differences may explain the disparate responses to therapy and clinical outcomes when comparing children and adults with HGG. The recently proposed integrated genomic classification identifies 6 distinct biological subgroups of glioblastoma (GBM) throughout the age spectrum. Driver mutations in genes affecting histone H3.3 (K27M and G34R/V) coupled with mutations involving specific proteins (TP53, ATRX, DAXX, SETD2, ACVR1, FGFR1, NTRK) induce defects in chromatin remodeling and may play a central role in the genesis of many pediatric HGGs. Current clinical practice in pediatric HGGs includes surgical resection followed by radiation therapy (in children aged > 3 years) with concurrent and adjuvant chemotherapy with temozolomide. However, these multimodality treatment strategies have had a minimal impact on improving survival. Ongoing clinical trials are investigating new molecular targets, chemoradiation sensitization strategies, and immunotherapy. Future clinical trials of pediatric HGG will incorporate the distinction between GBM molecular subgroups and stratify patients using group-specific biomarkers.

Indexed as

brain tumorglioblastomahigh-grade gliomapediatric

Identifiers

PMID26034626
PMCPMC4369714
OpenAlexW2136627211

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.