Evidence map›Paper›PMID 37314567›Full record

ArticleCellular and molecular life sciences : CMLS2023

CCL21-CCR7 signaling promotes microglia/macrophage recruitment and chemotherapy resistance in glioblastoma.

Luiz Henrique Geraldo, Celina Garcia, Yunling Xu, Felipe Saceanu Leser, Izabella Grimaldi, Eduardo Sabino de Camargo Magalhães, Joost Dejaegher, Lien Solie, Cláudia Maria Pereira, Ana Helena Correia and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.3field-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

21 citing papers in PubMed, 23 citations in OpenAlex.

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  6. Implications of Heterotypic Cell Fusion in Cancer.Advances in experimental medicine and biology · 2026
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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

17 authors at 4 institutions in 4 countries.

Luiz Henrique GeraldoLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil. luiz.geraldo@yale.edu.
Celina GarciaLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil.
Yunling XuUniversité de Paris, PARCC, INSERM, 75015, Paris, France.
Felipe Saceanu LeserLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil.
Izabella GrimaldiLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil.
Eduardo Sabino de Camargo MagalhãesLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil.
Joost DejaegherLaboratory of Experimental Neurosurgery and Neuroanatomy, Department of Neurosciences, KU Leuven, Leuven, Belgium.
Lien SolieLaboratory of Experimental Neurosurgery and Neuroanatomy, Department of Neurosciences, KU Leuven, Leuven, Belgium.
Cláudia Maria PereiraFaculdade de Odontologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, 21949-590, Brazil.
Ana Helena CorreiaDepartmento de Patologia, Faculdade de Medicina, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Steven De VleeschouwerLaboratory of Experimental Neurosurgery and Neuroanatomy, Department of Neurosciences, KU Leuven, Leuven, Belgium.
Bertrand TavitianUniversité de Paris, PARCC, INSERM, 75015, Paris, France.
Nathalie Henriques Silva CanedoDepartmento de Patologia, Faculdade de Medicina, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Thomas MathivetUniversité de Paris, PARCC, INSERM, 75015, Paris, France.
Jean-Leon ThomasUniversité Pierre et Marie Curie Paris 06 UMRS1127, Sorbonne Université, Paris, France. jean-leon.thomas@yale.edu.
Anne EichmannUniversité de Paris, PARCC, INSERM, 75015, Paris, France.
Flavia Regina Souza LimaLaboratório de Biologia das Células Gliais, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (UFRJ), Rua César Pernetta, 1.766, Cidade Universitária da UFRJ, Rio de Janeiro, RJ, 21949-590, Brazil. flaviareginasouzalima@gmail.com.ORCID http://orcid.org/0000-0003-0799-9235
Universidade Federal do Rio de Janeiro · BRInserm · FRKU Leuven · BEYale University · US

Funding

European Research Council 834161
6 · The paper itself

Abstract

Glioblastoma (GBM) is the most common and fatal primary tumor of the central nervous system (CNS) and current treatments have limited success. Chemokine signaling regulates both malignant cells and stromal cells of the tumor microenvironment (TME), constituting a potential therapeutic target against brain cancers. Here, we investigated the C-C chemokine receptor type 7 (CCR7) and the chemokine (C-C-motif) ligand 21 (CCL21) for their expression and function in human GBM and then assessed their therapeutic potential in preclinical mouse GBM models. In GBM patients, CCR7 expression positively associated with a poor survival. CCL21-CCR7 signaling was shown to regulate tumor cell migration and proliferation while also controlling tumor associated microglia/macrophage recruitment and VEGF-A production, thereby controlling vascular dysmorphia. Inhibition of CCL21-CCR7 signaling led to an increased sensitivity to temozolomide-induced tumor cell death. Collectively, our data indicate that drug targeting of CCL21-CCR7 signaling in tumor and TME cells is a therapeutic option against GBM.

Indexed as

GlioblastomaMicrogliaAnimalsCentral Nervous SystemChemokine CCL21HumansMacrophagesMiceReceptors, CCR7Tumor MicroenvironmentCCL21 protein, humanCCR7 protein, humanChemokine CCL21Receptors, CCR7ChemokinesTemozolomideTumor-associated microglia and macrophagesTumor microenvironmentVascular dysmorphia

Identifiers

PMID37314567
PMCPMC10267017
OpenAlexW4380576280

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.