Evidence map›Paper›PMID 30590711›Full record

ArticleNeuro-oncology2019

A non-hierarchical organization of tumorigenic NG2 cells in glioblastoma promoted by EGFR.

Talal F Al-Mayhani, Richard M Heywood, Vamsidhara Vemireddy, Justin D Lathia, Sara G M Piccirillo, Colin Watts

Open access · hybridAbstract read
In one paragraph

Article in Neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Microenvironmental Drivers of Glioma Progression.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. A Synopsis of Biomarkers in Glioblastoma: Past and Present.Current issues in molecular biology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Talal F Al-MayhaniBrain Repair Centre, University of Cambridge, Cambridge, UK.
Richard M HeywoodBrain Repair Centre, University of Cambridge, Cambridge, UK.
Vamsidhara VemireddyDepartment of Internal Medicine, Division of Hematology and Oncology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Justin D LathiaDepartment of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland, Ohio, USA.
Sara G M PiccirilloBrain Repair Centre, University of Cambridge, Cambridge, UK.
Colin WattsBrain Repair Centre, University of Cambridge, Cambridge, UK.
University of Cambridge · GBCleveland Clinic Lerner College of Medicine · USThe University of Texas Southwestern Medical Center · USUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExpression of neuron-glial antigen 2 (NG2) identifies an aggressive malignant phenotype in glioblastoma (GBM). Mouse models have implicated NG2 in the genesis, evolution, and maintenance of glial cancers and have highlighted potential interactions between NG2 and epidermal growth factor receptor (EGFR). However, it is unknown whether the lineage relationship of NG2+ and NG2- cells follows a hierarchical or stochastic mode of growth. Furthermore, the interaction between NG2 and EGFR signaling in human GBM is also unclear.

methodsSingle GBM NG2+ and NG2- cells were studied longitudinally to assess lineage relationships. Short hairpin RNA knockdown of NG2 was used to assess the mechanistic role of NG2 in human GBM cells. NG2+ and NG2- cells and NG2 knockdown (NG2-KD) and wild type (NG2-WT) cells were analyzed for differential effects on EGFR signaling.

resultsExpression of NG2 endows an aggressive phenotype both at single cell and population levels. Progeny derived from single GBM NG2- or GBM NG2+ cells consistently establish phenotypic equilibrium, indicating the absence of a cellular hierarchy. NG2 knockdown reduces proliferation, and mice grafted with NG2-KD survive longer than controls. Finally, NG2 promotes EGFR signaling and is associated with EGFR expression.

conclusionsThese data support a dynamic evolution in which a bidirectional relationship exists between GBM NG2+ and GBM NG2- cells. Such findings have implications for understanding phenotypic heterogeneity, the emergence of resistant disease, and developing novel therapeutics.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntigensApoptosisBiomarkers, TumorBrain NeoplasmsCarcinogenesisCell ProliferationChondroitin Sulfate Proteoglycan 4ErbB ReceptorsGlioblastomaHumansMiceProteoglycansSignal TransductionTumor Cells, CulturedAntigensBiomarkers, TumorChondroitin Sulfate Proteoglycan 4EGFR protein, humanErbB ReceptorsProteoglycansEGFR signalingglioblastomaNG2

Identifiers

PMID30590711
PMCPMC6765068
OpenAlexW2905633154

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.