Evidence map›Paper›PMID 25543125›Full record

ArticleNeuro-oncology2015

Inhibition of intracerebral glioblastoma growth by targeting the insulin-like growth factor 1 receptor involves different context-dependent mechanisms.

Martin Zamykal, Tobias Martens, Jakob Matschke, Hauke S Günther, Annegret Kathagen, Alexander Schulte, Regina Peters, Manfred Westphal, Katrin Lamszus

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuro-oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025
    Review
  7. Review
  8. Article
  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. Article
  16. Review
  17. Article
  18. 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

9 authors at 2 institutions in 1 country.

Martin ZamykalDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Tobias MartensDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Jakob MatschkeDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Hauke S GüntherDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Annegret KathagenDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Alexander SchulteDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Regina PetersDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Manfred WestphalDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
Katrin LamszusDepartment of Neurosurgery (M.Z., T.M., H.S.G., A.K., A.S., R.P., M.W., K.L.) and Institute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (J.M.).
University Medical Center Hamburg-Eppendorf · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSignaling by insulin-like growth factor 1 receptor (IGF-1R) can contribute to the formation and progression of many diverse tumor types, including glioblastoma. We investigated the effect of the IGF-1R blocking antibody IMC-A12 on glioblastoma growth in different in vivo models.

methodsU87 cells were chosen to establish rapidly growing, angiogenesis-dependent tumors in the brains of nude mice, and the GS-12 cell line was used to generate highly invasive tumors. IMC-A12 was administered using convection-enhanced local delivery. Tumor parameters were quantified histologically, and the functional relevance of IGF-1R activation was analyzed in vitro.

resultsIMC-A12 treatment inhibited the growth of U87 and GS-12 tumors by 75% and 50%, respectively. In GS-12 tumors, the invasive tumor extension and proliferation rate were significantly reduced by IMC-A12 treatment, while apoptosis was increased. In IMC-A12-treated U87 tumors, intratumoral vascularization was markedly decreased, and tumor cell proliferation was moderately reduced. Flow cytometry showed that <2% of U87 cells but >85% of GS-12 cells expressed IGF-1R. Activation of IGF-1R by IGF-1 and IGF-2 in GS-12 cells was blocked by IMC-A12. Both ligands stimulated GS-12 cell proliferation, and IGF-2 also stimulated migration. IMC-A12 inhibited these stimulatory effects and increased apoptosis. In U87 cells, stimulation with either ligand had no functional effect.

conclusionsIGF-1R blockade can inhibit glioblastoma growth by different mechanisms, including direct effects on the tumor cells as well as indirect anti-angiogenic effects. Hence, blocking IGF-1R may be useful to target both the highly proliferative, angiogenesis-dependent glioblastoma core component as well as the infiltrative periphery.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationGlioblastomaHumansInsulin-Like Growth Factor Binding Protein 1MiceNeovascularization, PathologicXenograft Model Antitumor AssaysAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedcixutumumabInsulin-Like Growth Factor Binding Protein 1angiogenesisconvection-enhanced deliverygliomaIGF-1Rinvasion

Identifiers

PMID25543125
PMCPMC4490867
OpenAlexW1988339729

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.