Evidence map›Paper›PMID 38087370›Full record

ReviewJournal of experimental & clinical cancer research : CR2023

Targeting the myeloid microenvironment in neuroblastoma.

Marjolein C Stip, Loes Teeuwen, Miranda P Dierselhuis, Jeanette H W Leusen, Daniëlle Krijgsman

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

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  20. Reprogramming the neuroblastoma tumor immune microenvironment to enhance GPC2 CAR T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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

5 authors at 2 institutions in 1 country.

Marjolein C StipCenter for Translational Immunology, University Medical Center Utrecht, 3584 CX, Utrecht, The Netherlands.
Loes TeeuwenCenter for Translational Immunology, University Medical Center Utrecht, 3584 CX, Utrecht, The Netherlands.
Miranda P DierselhuisPrincess Máxima Center for Pediatric Oncology, 3584 CS, Utrecht, The Netherlands.
Jeanette H W LeusenCenter for Translational Immunology, University Medical Center Utrecht, 3584 CX, Utrecht, The Netherlands.
Daniëlle KrijgsmanCenter for Translational Immunology, University Medical Center Utrecht, 3584 CX, Utrecht, The Netherlands. d.krijgsman-4@umcutrecht.nl.ORCID http://orcid.org/0000-0001-6101-7146
University Medical Center Utrecht · NLPrincess Máxima Center · NL

Funding

TKI-Health Holland TKI-2019
6 · The paper itself

Abstract

Myeloid cells (granulocytes and monocytes/macrophages) play an important role in neuroblastoma. By inducing a complex immunosuppressive network, myeloid cells pose a challenge for the adaptive immune system to eliminate tumor cells, especially in high-risk neuroblastoma. This review first summarizes the pro- and anti-tumorigenic functions of myeloid cells, including granulocytes, monocytes, macrophages, and myeloid-derived suppressor cells (MDSC) during the development and progression of neuroblastoma. Secondly, we discuss how myeloid cells are engaged in the current treatment regimen and explore novel strategies to target these cells in neuroblastoma. These strategies include: (1) engaging myeloid cells as effector cells, (2) ablating myeloid cells or blocking the recruitment of myeloid cells to the tumor microenvironment and (3) reprogramming myeloid cells. Here we describe that despite their immunosuppressive traits, tumor-associated myeloid cells can still be engaged as effector cells, which is clear in anti-GD2 immunotherapy. However, their full potential is not yet reached, and myeloid cell engagement can be enhanced, for example by targeting the CD47/SIRPα axis. Though depletion of myeloid cells or blocking myeloid cell infiltration has been proven effective, this strategy also depletes possible effector cells for immunotherapy from the tumor microenvironment. Therefore, reprogramming of suppressive myeloid cells might be the optimal strategy, which reverses immunosuppressive traits, preserves myeloid cells as effectors of immunotherapy, and subsequently reactivates tumor-infiltrating T cells.

Indexed as

Myeloid-Derived Suppressor CellsNeoplasmsNeuroblastomaHumansImmunotherapyMacrophagesMyeloid CellsTumor MicroenvironmentImmunosuppressionImmunotherapyMacrophagesMonocytesMyeloid cellsMyeloid-derived suppressor cellNeuroblastomaNeutrophils

Identifiers

PMID38087370
PMCPMC10716967
OpenAlexW4389639426

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.