Evidence map›Paper›PMID 27283525›Full record

ArticleJournal of neuro-oncology2016

Treatment with the PI3K inhibitor buparlisib (NVP-BKM120) suppresses the growth of established patient-derived GBM xenografts and prolongs survival in nude rats.

I A Netland, H E Førde, L Sleire, L Leiss, M A Rahman, B S Skeie, H Miletic, P Ø Enger, D Goplen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. ModularFrontiers in toxicology · 2026
    Article
  7. Article
  8. Review
  9. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Therapeutic Options in Neuro-Oncology.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Targeting PI3K/Akt signal transduction for cancer therapy.Signal transduction and targeted therapy · 2021
    Review
  16. Article
  17. Targeting RTK-PI3K-mTOR Axis in Gliomas: An Update.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Review
  20. Review
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

9 authors.

I A NetlandOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
H E FørdeOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
L SleireOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
L LeissOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
M A RahmanOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
B S SkeieDepartment of Clinical Medicine, K1, University of Bergen, Bergen, Norway.
H MileticDepartment of Biomedicine, Kristian Gerhard Jebsen Brain Tumour Research Center, University of Bergen, Bergen, Norway.
P Ø EngerOncomatrix Research Lab, Department of Biomedicine, University of Bergen, Bergen, Norway.
D GoplenDepartment of Biomedicine, Kristian Gerhard Jebsen Brain Tumour Research Center, University of Bergen, Bergen, Norway. dorota@goplen.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas (GBMs) are aggressive brain tumours with a dismal prognosis, despite combined surgery, radio- and chemotherapy. Close to 90 % of all GBMs harbour a deregulated PI3K pathway, which is essential in regulating central cellular functions such as proliferation, cell growth, motility and survival. Thus, PI3K represents a potential target for molecular therapy in GBM. We investigated the anti-tumour efficacy of the PI3K inhibitor buparlisib (NVP-BKM120) in GBM cell lines in vitro and in vivo, when treatment was initiated after MRI-confirmed tumour engraftment. We found that buparlisib inhibited glioma cell proliferation in a dose dependent manner, demonstrated by MTS assay, manual cell count and BrdU incorporation. A dose dependent increase in apoptosis was observed through flow cytometric analysis. Furthermore, by immunocytochemistry and western blot, we found a dose dependent inhibition of Akt phosphorylation. Moreover, buparlisib prolonged survival of nude rats harboring human GBM xenografts in three independent studies and reduced the tumours' volumetric increase, as determined by MRI. In addition, histological analyses of xenograft rat brains showed necrotic areas and change in tumour cell nuclei in buparlisib-treated animals. The rats receiving buparlisib maintained their weight, activity level and food- and water intake. In conclusion, buparlisib effectively inhibits glioma cell proliferation in vitro and growth of human GBM xenografts in nude rats. Moreover, the compound is well tolerated when administered at doses providing anti-tumour efficacy. Thus, buparlisib may have a future role in glioma therapy, and further studies are warranted to validate this compound for human use.

Indexed as

Phosphoinositide-3 Kinase InhibitorsXenograft Model Antitumor AssaysAminopyridinesAnimalsAntineoplastic AgentsApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationCell SurvivalGlioblastomaHumansMorpholinesPhosphorylationProto-Oncogene Proteins c-aktRats, NudeAminopyridinesAntineoplastic AgentsMorpholinesNVP-BKM120Phosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktBrain tumoursGlioblastomaPatient-derived xenograftPI3KProliferationTargeted therapy

Identifiers

PMID27283525
PMCPMC4972854

What OpenQuestion holds

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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.