Evidence map›Paper›PMID 31747383›Full record

ReviewRadiology and oncology2019

Cytokine CCL5 and receptor CCR5 axis in glioblastoma multiforme.

Miha Koprivnikar Kranjc, Metka Novak, Richard G Pestell, Tamara T Lah

Open access · goldAbstract readReview
In one paragraph

Review in Radiology and oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Pro- vs. Anti-Inflammatory Features of Monocyte Subsets in Glioma Patients.International journal of molecular sciences · 2023
    Article
  20. 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

4 authors at 3 institutions in 2 countries.

Miha Koprivnikar KranjcDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
Metka NovakDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
Richard G PestellPennsylvania Cancer and Regenerative Medicine Research Center, Baruch S. Blumberg Institute, Pennsylvania Biotechnology Center, Wynnewood, Pennsylvania,USA.
Tamara T LahDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Ljubljana, Slovenia.
National Institute of Biology · SIBaruch S. Blumberg Institute · USUniversity of Ljubljana · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Glioblastoma is the most frequent and aggressive brain tumour in humans with median survival from 12 to 15 months after the diagnosis. This is mostly due to therapy resistant glioblastoma stem cells in addition to intertumour heterogeneity that is due to infiltration of a plethora of host cells. Besides endothelial cells, mesenchymal stem cells and their differentiated progenies, immune cells of various differentiation states, including monocytes, comprise resident, brain tumour microenvironment. There are compelling evidence for CCL5/CCR5 in the invasive and metastatic behaviour of many cancer types. CCR5, a G-protein coupled receptor, known to function as an essential co-receptor for HIV entry, is now known to participate in driving tumour heterogeneity, the formation of cancer stem cells and the promotion of cancer invasion and metastasis. Clinical trials have recently opened targeting CCR5 using a humanized monoclonal antibody (leronlimab) for metastatic triple negative breast cancer (TNBC) or a small molecule inhibitor (maraviroc) for metastatic colon cancer. There are important CCL5 and CCR5 structure and signalling mechanisms in glioblastoma. In addition, the CCL5/CCR5 axis directs infiltration and interactions with monocytes/macrophages and mesenchymal stem cells, comprising glioblastoma stem cell niches. Conclusions CCR5 is highly expressed in glioblastoma and is associated with poor prognosis of patients. CCL5/CCR5 is suggested to be an excellent new target for glioblastoma therapy. The molecular mechanisms, by which chemoattractant and receptor respond within the complex tissue microenvironment to promote cancer stem cells and tumour heterogeneity, should be considered in forthcoming studies.

Indexed as

Brain NeoplasmsCCR5 Receptor AntagonistsChemokine CCL5Disease ProgressionGene Expression Regulation, NeoplasticGlioblastomaHumansMolecular Targeted TherapyNeoplasm MetastasisReceptors, CCR5Tumor MicroenvironmentCCL5 protein, humanCCR5 protein, humanCCR5 Receptor AntagonistsChemokine CCL5Receptors, CCR5CCL5-RANTEScytokinesglioblastomamesenchymal stem cellssignallingtumour microenvironment

Identifiers

PMID31747383
PMCPMC6884928
OpenAlexW2990519108

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.