Evidence map›Paper›PMID 23324350›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Sorafenib selectively depletes human glioblastoma tumor-initiating cells from primary cultures.

Elisa Carra, Federica Barbieri, Daniela Marubbi, Alessandra Pattarozzi, Roberto E Favoni, Tullio Florio, Antonio Daga

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
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  12. Review
  13. Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  14. αvβ3-integrin regulates PD-L1 expression and is involved in cancer immune evasion.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Review
  16. Review
  17. Article
  18. Translational gap in ongoing clinical trials for glioma.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2018
    Review
  19. 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

7 authors at 4 institutions in 3 countries.

Elisa CarraDepartment of Experimental Medicine (DIMES), University of Genova, Genova, Italy.
Federica Barbieri
Daniela Marubbi
Alessandra Pattarozzi
Roberto E Favoni
Tullio Florio
Antonio Daga
University of Genoa · ITOspedale Policlinico San Martino · ITAlleanza Contro il Cancro · ITInstitute of Pharmacology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas are grade IV brain tumors characterized by high aggressiveness and invasiveness, giving patients a poor prognosis. We investigated the effects of the multi-kinase inhibitor sorafenib on six cultures isolated from human glioblastomas and maintained in tumor initiating cells-enriching conditions. These cell subpopulations are thought to be responsible for tumor recurrence and radio- and chemo-resistance, representing the perfect target for glioblastoma therapy. Sorafenib reduces proliferation of glioblastoma cultures, and this effect depends, at least in part, on the inhibition of PI3K/Akt and MAPK pathways, both involved in gliomagenesis. Sorafenib significantly induces apoptosis/cell death via downregulation of the survival factor Mcl-1. We provide evidence that sorafenib has a selective action on glioblastoma stem cells, causing enrichment of cultures in differentiated cells, downregulation of the expression of stemness markers required to maintain malignancy (nestin, Olig2 and Sox2) and reducing cell clonogenic ability in vitro and tumorigenic potential in vivo. The selectivity of sorafenib effects on glioblastoma stem cells is confirmed by the lower sensitivity of glioblastoma cultures after differentiation as compared with the undifferentiated counterpart. Since current GBM therapy enriches the tumor in cancer stem cells, the evidence of a selective action of sorafenib on these cells is therapeutically relevant, even if, so far, results from first phase II clinical trials did not demonstrate its efficacy.

Indexed as

ApoptosisBasic Helix-Loop-Helix ProteinsBrain NeoplasmsCell DifferentiationCell ProliferationDown-RegulationGlioblastomaHumansIntermediate Filament ProteinsMitogen-Activated Protein KinasesMyeloid Cell Leukemia Sequence 1 ProteinNeoplastic Stem CellsNerve Tissue ProteinsNestinNiacinamideOligodendrocyte Transcription Factor 2Basic Helix-Loop-Helix ProteinsIntermediate Filament ProteinsMitogen-Activated Protein KinasesMyeloid Cell Leukemia Sequence 1 ProteinNerve Tissue ProteinsNES protein, humanNestinNiacinamideOLIG2 protein, humanOligodendrocyte Transcription Factor 2Phenylurea CompoundsPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2SorafenibSOX2 protein, humanSOXB1 Transcription FactorsSTAT3 protein, humanSTAT3 Transcription FactorglioblastomaMcl-1sorafenibstemnesstherapytumor initiating cells

Identifiers

PMID23324350
PMCPMC3587450
OpenAlexW2068889110

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.