Evidence map›Paper›PMID 29867979›Full record

ReviewFrontiers in immunology2018

Immune Microenvironment in Glioblastoma Subtypes.

Zhihong Chen, Dolores Hambardzumyan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 285 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
285citing papers in PubMed, 1 pooled it
16.3field-weighted citation impact, top 1% 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

285 citing papers in PubMed, 1 synthesis or guideline pooled it, 424 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  5. Review
  6. Review
  7. Article
  8. Article
  9. Microstructure mapping with time-dependent diffusion MRI differentiates primary central nervous system lymphoma from glioblastoma.Cancer imaging : the official publication of the International Cancer Imaging Society · 2026
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

225 more citing papers are in PubMed but not listed here.

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.

Zhihong ChenDepartment of Pediatrics, Aflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, United States.
Dolores HambardzumyanDepartment of Pediatrics, Aflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, United States.
Children's Healthcare of Atlanta · USEmory University · US

Funding

Tumor-Associated Macrophages in Vasogenic Cerebral Edema in Brain TumorsR01NS100864 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Dolores Hambardzumyan · 2017 to 2026
$5.4M
Non-neoplastic cell types dictate gliomagenesis andU01CA160882 · NCI · EMORY UNIVERSITY · PI HAMBARDZUMYAN, DOLORES, HOLLAND, ERIC C. · 2012 to 2016
$2.8M
NCI NIH HHS U01 CA160882NINDS NIH HHS R01 NS100864
6 · The paper itself

Abstract

Glioblastomas (GBMs) are the most common and aggressive primary brain tumors. Due to their malignant growth and invasion into the brain parenchyma coupled with resistance to therapy, GBMs are among the deadliest of all cancers. GBMs are highly heterogeneous at both the molecular and histological levels. Hallmark histological structures include pseudopalisading necrosis and microvascular proliferation. In addition to high levels of intratumoral heterogeneity, GBMs also exhibit high levels of inter-tumoral heterogeneity. The major non-neoplastic cell population in the GBM microenvironment includes cells of the innate immune system called tumor-associated macrophages (TAMs). Correlative data from the literature suggest that molecularly distinct GBM subtypes exhibit differences in their microenvironment. Data from mouse models of GBM suggest that genetic driver mutations can create unique microenvironments. Here, we review the origin, features, and functions of TAMs in distinct GBM subtypes. We also discuss their interactions with other immune cell constituents and discuss prospects of therapeutically targeting TAMs to increase the efficacy of T-cell functions.

Indexed as

AnimalsBrain NeoplasmsDisease Models, AnimalGlioblastomaHumansImmunity, InnateImmunotherapyMacrophagesMiceMutationTumor Microenvironmentglioblastomaimmunotherapymacrophagesmicrogliatumor-associated macrophagestumor microenvironment

Identifiers

PMID29867979
PMCPMC5951930
OpenAlexW2799441834

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.