Evidence map›Paper›PMID 36212415›Full record

ReviewFrontiers in oncology2022

Exploring glioblastoma stem cell heterogeneity: Immune microenvironment modulation and therapeutic opportunities.

Amanda L Johnson, John Laterra, Hernando Lopez-Bertoni

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  14. Advancements in nanotheranostics for glioma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
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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

3 authors at 3 institutions in 1 country.

Amanda L JohnsonHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, United States.
John LaterraHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, United States.
Hernando Lopez-BertoniHugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD, United States.
Johns Hopkins Medicine · USJohns Hopkins University · USKennedy Krieger Institute · US

Funding

Chromatin Modifications in GBM-Propagating CellsR01NS096754 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2017 to 2021
$2.2M
Molecular determinants of cellular heterogeneity and therapeutic resistance in GBM.R01NS120949 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LOPEZ-BERTONI, HERNANDO MARTIN · 2021 to 2025
$2.0M
Tet2 regulation and function in glioma cell phenotype reprogrammingR01NS110087 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2019 to 2023
$1.8M
NINDS NIH HHS R01 NS096754NINDS NIH HHS R01 NS110087NINDS NIH HHS R01 NS120949
6 · The paper itself

Abstract

Despite its growing use in cancer treatment, immunotherapy has been virtually ineffective in clinical trials for gliomas. The inherently cold tumor immune microenvironment (TIME) in gliomas, characterized by a high ratio of pro-tumor to anti-tumor immune cell infiltrates, acts as a seemingly insurmountable barrier to immunotherapy. Glioma stem cells (GSCs) within these tumors are key contributors to this cold TIME, often functioning indirectly through activation and recruitment of pro-tumor immune cell types. Furthermore, drivers of GSC plasticity and heterogeneity (e.g., reprogramming transcription factors, epigenetic modifications) are associated with induction of immunosuppressive cell states. Recent studies have identified GSC-intrinsic mechanisms, including functional mimicry of immune suppressive cell types, as key determinants of anti-tumor immune escape. In this review, we cover recent advancements in our understanding of GSC-intrinsic mechanisms that modulate GSC-TIME interactions and discuss cutting-edge techniques and bioinformatics platforms available to study immune modulation at high cellular resolution with exploration of both malignant (i.e., GSC) and non-malignant (i.e., immune) cell fractions. Finally, we provide insight into the therapeutic opportunities for targeting immunomodulatory GSC-intrinsic mechanisms to potentiate immunotherapy response in gliomas.

Indexed as

cancer stem cellcancer therapycellular mimicryimmunomodulationmulti omicssingle-cell sequencingspatial analysis

Identifiers

PMID36212415
PMCPMC9532940
OpenAlexW4296745094

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.