Evidence map›Paper›PMID 39395421›Full record

ArticleImmunity2024

Microglia and monocyte-derived macrophages drive progression of pediatric high-grade gliomas and are transcriptionally shaped by histone mutations.

James L Ross, Montserrat Puigdelloses-Vallcorba, Gonzalo Piñero, Nishant Soni, Wes Thomason, John DeSisto, Angelo Angione, Nadejda M Tsankova, Maria G Castro, Matthew Schniederjan and 7 more

Abstract read
In one paragraph

Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  14. Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

James L RossDepartment of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA, USA.
Montserrat Puigdelloses-VallcorbaDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA.
Gonzalo PiñeroDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA.
Nishant SoniDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Wes ThomasonDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA.
John DeSistoMorgan Adams Foundation Pediatric Brain Tumor Research Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Cell Biology, Stem Cells and Development Graduate Program, Aurora, CO, USA; Center for Cancer and Blood Disorders, Children's Hospital Colorado, Aurora, CO, USA.
Angelo AngioneDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA.
Nadejda M TsankovaDepartment of Pathology and Molecular and Cell-Based Medicine, Mount Sinai Icahn School of Medicine, New York, NY 10029, USA.
Maria G CastroDepartments of Neurosurgery and Cell & Developmental Biology, The University of Michigan School of Medicine, Ann Arbor, MI, USA.
Matthew SchniederjanDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA.
Nitin R WadhwaniDepartment of Pathology and Laboratory Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
G Praveen RajuDepartment of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Peter MorgensternDepartment of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA.
Oren J BecherDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Adam L GreenMorgan Adams Foundation Pediatric Brain Tumor Research Program, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Cell Biology, Stem Cells and Development Graduate Program, Aurora, CO, USA; Center for Cancer and Blood Disorders, Children's Hospital Colorado, Aurora, CO, USA.
Alexander M TsankovDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Dolores HambardzumyanDepartment of Oncological Sciences, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Neurosurgery, Mount Sinai Icahn School of Medicine, New York, NY, USA. Electronic address: dolores.hambardzumyan@mssm.edu.

Funding

Tumor-Associated Macrophages in Vasogenic Cerebral Edema in Brain TumorsR01NS100864 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Dolores Hambardzumyan · 2017 to 2026
$5.4M
The role of Myeloid cells in pediatric-high grade gliomasR01CA258636 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BECHER, OREN JOSH, HAMBARDZUMYAN, DOLORES · 2022 to 2025
$2.7M
PDGF signaling in pediatric brain tumorsR21NS106554 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HAMBARDZUMYAN, DOLORES · 2018 to 2019
$422k
The Role of Tumor Associated Macrophages in Pediatric High-Grade GliomaF31CA232531 · NCI · EMORY UNIVERSITY · PI ROSS, JAMES LUKE · 2018 to 2019
$74k
NCI NIH HHS F31 CA232531NCI NIH HHS R01 CA258636NINDS NIH HHS R01 NS100864NINDS NIH HHS R21 NS106554
6 · The paper itself

Abstract

Pediatric high-grade gliomas (pHGGs), including hemispheric pHGGs and diffuse midline gliomas (DMGs), harbor mutually exclusive tumor location-specific histone mutations. Using immunocompetent de novo mouse models of pHGGs, we demonstrated that myeloid cells were the predominant infiltrating non-neoplastic cell population. Single-cell RNA sequencing (scRNA-seq), flow cytometry, and immunohistochemistry illustrated the presence of heterogeneous myeloid cell populations shaped by histone mutations and tumor location. Disease-associated myeloid (DAM) cell phenotypes demonstrating immune permissive characteristics were identified in murine and human pHGG samples. H3.3K27M DMGs, the most aggressive DMG, demonstrated enrichment of DAMs. Genetic ablation of chemokines Ccl8 and Ccl12 resulted in a reduction of DAMs and an increase in lymphocyte infiltration, leading to increased survival of tumor-bearing mice. Pharmacologic inhibition of chemokine receptors CCR1 and CCR5 resulted in extended survival and decreased myeloid cell infiltration. This work establishes the tumor-promoting role of myeloid cells in DMG and the potential therapeutic opportunities for targeting them.

Indexed as

Brain NeoplasmsDisease ProgressionGliomaHistonesMacrophagesMicrogliaMutationAnimalsChildDisease Models, AnimalHumansMiceMice, Inbred C57BLMyeloid CellsReceptors, CCR1Receptors, CCR5Ccr1 protein, mouseHistonesReceptors, CCR1Receptors, CCR5CCR1CCR5diffuse midline gliomadisease-associated macrophagehigh-grade gliomamacrophagemicrogliamonocytepediatric gliomaTAM

Identifiers

PMID39395421
PMCPMC11578068

What OpenQuestion holds

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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.