Evidence map›Paper›PMID 33919732›Full record

ReviewCells2021

New Insights into the Multifaceted Role of Myeloid-Derived Suppressor Cells (MDSCs) in High-Grade Gliomas: From Metabolic Reprograming, Immunosuppression, and Therapeutic Resistance to Current Strategies for Targeting MDSCs.

Senthilnath Lakshmanachetty, Joselyn Cruz-Cruz, Eric Hoffmeyer, Allison P Cole, Siddhartha S Mitra

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. CD13 identifies S100A4Biology direct · 2026
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  9. KITENIN-CCL20 axis is a potential therapeutic target for modulating immunosuppressive tumor microenvironment in glioblastoma.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 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

5 authors at 1 institution in 1 country.

Senthilnath LakshmanachettyMorgan Adams Brain Tumor Research Program, Department of Pediatrics, Division of Hematology/Oncology/Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0002-3760-2772
Joselyn Cruz-CruzMorgan Adams Brain Tumor Research Program, Department of Pediatrics, Division of Hematology/Oncology/Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.ORCID 0000-0003-2760-3648
Eric HoffmeyerMorgan Adams Brain Tumor Research Program, Department of Pediatrics, Division of Hematology/Oncology/Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Allison P ColeMorgan Adams Brain Tumor Research Program, Department of Pediatrics, Division of Hematology/Oncology/Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Siddhartha S MitraMorgan Adams Brain Tumor Research Program, Department of Pediatrics, Division of Hematology/Oncology/Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Morgan Adams Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells "hijack" host immune cells to promote growth, survival, and metastasis. The immune microenvironment of high-grade gliomas (HGG) is a complex and heterogeneous system, consisting of diverse cell types such as microglia, bone marrow-derived macrophages (BMDMs), myeloid-derived suppressor cells (MDSCs), dendritic cells, natural killer (NK) cells, and T-cells. Of these, MDSCs are one of the major tumor-infiltrating immune cells and are correlated not only with overall worse prognosis but also poor clinical outcomes. Upon entry from the bone marrow into the peripheral blood, spleen, as well as in tumor microenvironment (TME) in HGG patients, MDSCs deploy an array of mechanisms to perform their immune and non-immune suppressive functions. Here, we highlight the origin, function, and characterization of MDSCs and how they are recruited and metabolically reprogrammed in HGG. Furthermore, we discuss the mechanisms by which MDSCs contribute to immunosuppression and resistance to current therapies. Finally, we conclude by summarizing the emerging approaches for targeting MDSCs alone as a monotherapy or in combination with other standard-of-care therapies to improve the current treatment of high-grade glioma patients.

Indexed as

Drug Resistance, NeoplasmImmunosuppression TherapyBrain NeoplasmsGliomaHumansMyeloid-Derived Suppressor CellsNeoplasm Gradingbrain tumorsglioblastomagliomahigh-grade gliomaimmune suppressionimmunotherapyMDSCsmetabolic reprogrammingtherapeutic resistancetherapeutic targetingtumor microenvironment

Identifiers

PMID33919732
PMCPMC8070707
OpenAlexW3153242172

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.