Evidence map›Paper›PMID 17506723›Full record

ArticleThe Biochemical journal2007

Novel role for insulin as an autocrine growth factor for malignant brain tumour cells.

Alexandre Arcaro, Kathrin T Doepfner, Danielle Boller, Ana S Guerreiro, Tarek Shalaby, Shaun P Jackson, Simone M Schoenwaelder, Olivier Delattre, Michael A Grotzer, Barbara Fischer

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. MEK Inhibition Suppresses Growth of Atypical Teratoid/Rhabdoid Tumors.Journal of neuropathology and experimental neurology · 2020
    Article
  4. Article
  5. Article
  6. Insulin Receptor Isoforms in Cancer.International journal of molecular sciences · 2018
    Review
  7. Atypical Teratoid Rhabdoid Tumour : From Tumours to Therapies.Journal of Korean Neurosurgical Society · 2018
    Review
  8. Article
  9. Review
  10. InsR/IGF1R Pathway Mediates Resistance to EGFR Inhibitors in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

10 authors at 3 institutions in 3 countries.

Alexandre ArcaroDivision of Clinical Chemistry and Biochemistry, University Children's Hospital Zurich, CH-8032 Zurich, Switzerland. Alexandre.Arcaro@kispi.unizh.ch
Kathrin T Doepfner
Danielle Boller
Ana S Guerreiro
Tarek Shalaby
Shaun P Jackson
Simone M Schoenwaelder
Olivier Delattre
Michael A Grotzer
Barbara Fischer
University Children's Hospital Zurich · CHMonash University · AUInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AT/RTs (atypical teratoid/rhabdoid tumours) of the CNS (central nervous system) are childhood malignancies associated with poor survival rates due to resistance to conventional treatments such as chemotherapy. We characterized a panel of human AT/RT and MRT (malignant rhabdoid tumour) cell lines for expression of RTKs (receptor tyrosine kinases) and their involvement in tumour growth and survival. When compared with normal brain tissue, AT/RT cell lines overexpressed the IR (insulin receptor) and the IGFIR (insulin-like growth factor-I receptor). Moreover, insulin was secreted by AT/RT cells grown in serum-free medium. Insulin potently activated Akt (also called protein kinase B) in AT/RT cells, as compared with other growth factors, such as epidermal growth factor. Pharmacological inhibitors, neutralizing antibodies, or RNAi (RNA interference) targeting the IR impaired the growth of AT/RT cell lines and induced apoptosis. Inhibitors of the PI3K (phosphoinositide 3-kinase)/Akt pathway also impaired basal and insulin-stimulated AT/RT cell proliferation. Experiments using RNAi and isoform-specific pharmacological inhibitors established a key role for the class I(A) PI3K p110alpha isoform in AT/RT cell growth and insulin signalling. Taken together, our results reveal a novel role for autocrine signalling by insulin and the IR in growth and survival of malignant human CNS tumour cells via the PI3K/Akt pathway.

Indexed as

Autocrine CommunicationBrain NeoplasmsCell Line, TumorCell ProliferationChild, PreschoolChromosomal Proteins, Non-HistoneCulture Media, Serum-FreeDNA-Binding ProteinsDown-RegulationEnzyme ActivationFemaleGrowth SubstancesHumansInfantInsulinInsulin SecretionChromosomal Proteins, Non-HistoneCulture Media, Serum-FreeDNA-Binding ProteinsGrowth SubstancesInsulinIsoenzymesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptor, InsulinRNA, Small InterferingSMARCB1 ProteinSMARCB1 protein, humanTranscription Factors

Identifiers

PMID17506723
PMCPMC1948991
OpenAlexW2001172791

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.