Evidence map›Paper›PMID 18682579›Full record

ArticleNeuro-oncology2009

Efficacy of the HSP90 inhibitor 17-AAG in human glioma cell lines and tumorigenic glioma stem cells.

Claire Marie-Elisabeth Sauvageot, Jessica Leigh Weatherbee, Santosh Kesari, Susan Elizabeth Winters, Jessica Barnes, Jamie Dellagatta, Naren Raj Ramakrishna, Charles Dean Stiles, Andrew Li-Jen Kung, Mark W Kieran and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

67 citing papers in PubMed, 145 citations in OpenAlex.

  1. Article
  2. Review
  3. In vivo generation of CAR macrophages via the enucleated mesenchymal stem cell delivery system for glioblastoma therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  11. Antitumor Activity of a Mitochondrial-Targeted HSP90 Inhibitor in Gliomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  12. Article
  13. HSP90-CDC37 functions as a chaperone for the oncogenic FGFR3-TACC3 fusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
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  14. Article
  15. Review
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7 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 1 country.

Claire Marie-Elisabeth SauvageotDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115. claire_sauvageot@dfci.harvard.edu
Jessica Leigh Weatherbee
Santosh Kesari
Susan Elizabeth Winters
Jessica Barnes
Jamie Dellagatta
Naren Raj Ramakrishna
Charles Dean Stiles
Andrew Li-Jen Kung
Mark W Kieran
Patrick Yung Chih Wen
Brigham and Women's Hospital · USDana-Farber Cancer Institute · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) arises from genetic and signaling abnormalities in components of signal transduction pathways involved in proliferation, survival, and the cell cycle axis. Studies to date with single-agent targeted molecular therapy have revealed only modest effects in attenuating the growth of these tumors, suggesting that targeting multiple aberrant pathways may be more beneficial. Heat-shock protein 90 (HSP90) is a molecular chaperone that is involved in the conformational maturation of a defined group of client proteins, many of which are deregulated in GBM. 17-allylamino-17-demethoxygeldanamycin (17-AAG) is a well-characterized HSP90 inhibitor that should be able to target many of the aberrant signal transduction pathways in GBM. We assessed the ability of 17-AAG to inhibit the growth of glioma cell lines and glioma stem cells both in vitro and in vivo and assessed its ability to synergize with radiation and/or temozolomide, the standard therapies for GBM. Our results reveal that 17-AAG is able to inhibit the growth of both human glioma cell lines and glioma stem cells in vitro and is able to target the appropriate proteins within these cells. In addition, 17-AAG can inhibit the growth of intracranial tumors and can synergize with radiation both in tissue culture and in intracranial tumors. This compound was not found to synergize with temozolomide in any of our models of gliomas. Our results suggest that HSP90 inhibitors like 17-AAG may have therapeutic potential in GBM, either as a single agent or in combination with radiation.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingBenzoquinonesBlotting, WesternBrain NeoplasmsCell Line, TumorDacarbazineDrug Therapy, CombinationErbB ReceptorsGliomaHSP90 Heat-Shock ProteinsHumansLactams, MacrocyclicMiceMice, NudeMice, SCIDAntineoplastic Agents, AlkylatingBenzoquinonesDacarbazineEGFR protein, humanErbB ReceptorsHSP90 Heat-Shock ProteinsLactams, MacrocyclicPTEN PhosphohydrolasePTEN protein, humantanespimycinTemozolomideTumor Suppressor Protein p53

Identifiers

PMID18682579
PMCPMC2718982
OpenAlexW2012172048

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.