Evidence map›Paper›PMID 31650201›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2020

Insights in the immunobiology of glioblastoma.

Dimitrios Strepkos, Mariam Markouli, Alexia Klonou, Christina Piperi, Athanasios G Papavassiliou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2020. 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
3.3field-weighted citation impact, top 7% 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, 72 citations in OpenAlex.

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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.

Dimitrios StrepkosDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street-Bldg 16, 115 27, Athens, Greece.
Mariam MarkouliDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street-Bldg 16, 115 27, Athens, Greece.
Alexia KlonouDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street-Bldg 16, 115 27, Athens, Greece.
Christina PiperiDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street-Bldg 16, 115 27, Athens, Greece. cpiperi@med.uoa.gr.
Athanasios G PapavassiliouDepartment of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street-Bldg 16, 115 27, Athens, Greece. papavas@med.uoa.gr.ORCID 0000-0001-5803-4527
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma, a grade IV astrocytoma, is considered as the most malignant intracranial tumor, characterized by poor prognosis and therapy resistance. Tumor heterogeneity that often leads to distinct functional phenotypes contributes to glioblastoma (GB) indispensable growth and aggressiveness. The complex interaction of neoplastic cells with tumor microenvironment (TME) along with the presence of cancer stem-like cells (CSCs) largely confers to extrinsic and intrinsic GB heterogeneity. Recent data indicate that glioma cells secrete a variety of soluble immunoregulatory factors to attract different cell types to TME including astrocytes, endothelial cells, circulating stem cells, and a range of immune cells. These further induce a local production of cytokines, chemokines, and growth factors which upon crosstalk with extracellular matrix (ECM) components reprogram immune cells to inflammatory or anti-inflammatory phenotypes and manipulate host's immune response in favor of cancer growth and metastasis. Herein, we provide an overview of the immunobiologic factors that orchestrate the complex network of glioma cells and TME interactions in an effort to identify potential therapeutic targets for GB malignancy. Current therapeutic schemes and advances in targeting GB-TME crosstalk are further discussed. KEY MESSAGES: • Intrinsic and extrinsic tumor heterogeneity affects GB growth and aggressiveness. • GB cells secrete growth factors and chemoattractants to recruit immune cells to TME. • GAMs are a critical cell type in promoting GB growth. • GAMs change from pro-inflammatory, anti-tumor M1 phenotype to pro-tumorigenic M2. • Novel therapeutic agents target the crosstalk of neoplastic cells with TME.

Indexed as

AdultAgedAged, 80 and overAnimalsBrain NeoplasmsChildCytokinesFemaleGenetic HeterogeneityGlioblastomaHumansMacrophagesMaleMiceMicrogliaMiddle AgedCytokinesChemokinesCytokinesGAMsGliomasImmunotherapyVaccines

Identifiers

PMID31650201
OpenAlexW2981956166

What OpenQuestion holds

Textmetadata
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.