Evidence map›Paper›PMID 29427211›Full record

ArticleJournal of cancer research and clinical oncology2018

Treatment with 5-azacitidine delay growth of glioblastoma xenografts: a potential new treatment approach for glioblastomas.

Tobias Kratzsch, Susanne Antje Kuhn, Andreas Joedicke, Uwe Karsten Hanisch, Peter Vajkoczy, Jens Hoffmann, Iduna Fichtner

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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 5 institutions in 1 country.

Tobias KratzschDepartment of Neurosurgery, Charité University Hospital, Chariteplatz 1, 10117, Berlin, Germany. tobias.kratzsch@charite.de.ORCID http://orcid.org/0000-0002-3996-0418
Susanne Antje KuhnDepartment of Neurosurgery, Ernst von Bergmann Hospital, Potsdam, Germany.
Andreas JoedickeDepartment of Neurosurgery, Vivantes Hospital Berlin Neukölln, Berlin, Germany.
Uwe Karsten HanischInstitute of Neuropathology, University Hospital, Göttingen, Germany.
Peter VajkoczyDepartment of Neurosurgery, Charité University Hospital, Chariteplatz 1, 10117, Berlin, Germany.
Jens HoffmannExperimental Pharmacology and Oncology GmbH, Berlin, Germany.
Iduna FichtnerMax Delbrueck Center for Molecular Medicine, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DEKlinikum Ernst von Bergmann · DELeipzig University · DEMax Delbrück Center · DEVivantes Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGlioblastoma multiforme (GBM) is the most lethal primary brain tumor in adults. The epigenetically active ribonucleoside analog 5-azacitidine is a new therapy option that changes tumor cell chromatin, which is frequently modified by methylation and deacetylation in malignant gliomas.

methodsIn vitro, we analyzed cell viability, cell apoptosis, and migration of human GBM cells. In vivo, we established subcutaneous and intracerebral GBM mouse models originating from U87MG, U373MG, and primary GBM cells as well as one patient-derived xenograft. Xenografts were treated with 5-azacitidine as well as valproic acid, bevacizumab, temozolomide, and phosphate buffered saline. The tumor sizes and Ki67 proliferation indices were determined. Glioma angiogenesis was examined immunohistochemically by expression analysis of endothelial cells (CD31) and pericytes (PDGFRβ).

resultsIn vitro, 5-azacitidine treatment significantly reduced human glioblastoma cell viability, increased cellular apoptosis, and reduced cellular migration. In vivo, 5-azacitidine significantly reduced growth in two intracerebral GBM models. Notably, this was also shown for a xenograft established from a patient surgery sample; whereas, epigenetically acting valproic acid did not show any growth reduction. Highly vascularized tumors responded to treatment, whereas low-vascularized xenografts showed no response. Furthermore, intracerebral glioblastomas treated with 5-azacitidine showed a clearly visible reduction of tumor angiogenesis and lower numbers of endothelial cells and tumor vessel pericytes.

conclusionsOur data show significant growth inhibition as well as antiangiogenic effects in intracerebral as well as patient-derived GBM xenografts. This encourages to investigate in detail the multifactorial effects of 5-azacitidine on glioblastomas.

Indexed as

Xenograft Model Antitumor AssaysAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisAzacitidineBrain NeoplasmsCell Line, TumorCell MovementCell SurvivalFemaleGlioblastomaHumansMice, Inbred NODMice, KnockoutMice, NudeMice, SCIDAzacitidine5-AzacitidineEpigeneticsGlioblastomaTemozolomideValproic acidXenografts

Identifiers

PMID29427211
PMCPMC11813281
OpenAlexW2792849347

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.