Evidence map›Paper›PMID 26019225›Full record

ArticleStem cells translational medicine2015

CD15 Expression Does Not Identify a Phenotypically or Genetically Distinct Glioblastoma Population.

Emma Kenney-Herbert, Talal Al-Mayhani, Sara G M Piccirillo, Joanna Fowler, Inmaculada Spiteri, Philip Jones, Colin Watts

Open access · goldAbstract read
In one paragraph

Article in Stem cells translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025
    Review
  2. Review
  3. Article
  4. Glioma Stem Cells: Novel Data Obtained by Single-Cell Sequencing.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Opportunities and challenges of glioma organoids.Cell communication and signaling : CCS · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. 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

7 authors at 2 institutions in 1 country.

Emma Kenney-HerbertJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom cw209@cam.ac.uk emmakenneyherbert@yahoo.co.uk.
Talal Al-MayhaniJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom.
Sara G M PiccirilloJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom.
Joanna FowlerJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom.
Inmaculada SpiteriJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom.
Philip JonesJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom.
Colin WattsJohn van Geest Centre for Brain Repair, Department of Clinical Neurosciences, Cambridge University, Cambridge, United Kingdom; MRC Cancer Unit, Hutchison/MRC Research Centre, University of Cambridge, Cambridge, United Kingdom; The Institute of Cancer Research, London, United Kingdom cw209@cam.ac.uk emmakenneyherbert@yahoo.co.uk.
University of Cambridge · GBInstitute of Cancer Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelled: Recent research has focused on the hypothesis that the growth and regeneration of glioblastoma (GB) is sustained by a subpopulation of self-renewing stem-like cells. This has led to the prediction that molecular markers for cancer stem cells in GB may provide a treatment target. One candidate marker is CD15: we wanted to determine if CD15 represented a credible stem cell marker in GB. We first demonstrated that CD15-positive (CD15+) cells were less proliferative than their CD15-negative (CD15-) counterparts in 10 patient GB tumors. Next we compared the proliferative activity of CD15+ and CD15- cells in vitro using tumor-initiating primary GB cell lines (TICs) and found no difference in proliferative behavior. Furthermore, TICs sorted for CD15+ and CD15- were not significantly different cytogenetically or in terms of gene expression profile. Sorted single CD15+ and CD15- cells were equally capable of reconstituting a heterogeneous population containing both CD15+ and CD15- cells over time, and both CD15+ and CD15- cells were able to generate tumors in vivo. No difference was found in the phenotypic or genomic behavior of CD15+ cells compared with CD15- cells from the same patient. Moreover, we found that in vitro, cells were able to interconvert between the CD15+ and CD15- states. Our data challenge the utility of CD15 as a cancer stem cell marker. SIGNIFICANCE: The data from this study contribute to the ongoing debate about the role of cancer stem cells in gliomagenesis. Results showed that CD15, a marker previously thought to be a cancer stem-like marker in glioblastoma, could not isolate a phenotypically or genetically distinct population. Moreover, isolated CD15-positive and -negative cells were able to generate mixed populations of glioblastoma cells in vitro.

Indexed as

CancerCD15GlioblastomaHierarchySSEA1Stem cell

Identifiers

PMID26019225
PMCPMC4479614
OpenAlexW2169370347

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.