Evidence map›Paper›PMID 23714726›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Therapeutic potential of HSP90 inhibition for neurofibromatosis type 2.

Karo Tanaka, Ascia Eskin, Fabrice Chareyre, Walter J Jessen, Jan Manent, Michiko Niwa-Kawakita, Ruihong Chen, Cory H White, Jeremie Vitte, Zahara M Jaffer and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. 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
2.2field-weighted citation impact, top 12% 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, 43 citations in OpenAlex.

  1. Deletion of themBio · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Culture of attenuatedHuman vaccines & immunotherapeutics · 2023
    Article
  6. Review
  7. Intratumoral injection of schwannoma with attenuatedProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. A Critical Overview of Targeted Therapies for Vestibular Schwannoma.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. CNS Tumors in Neurofibromatosis.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017
    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

13 authors at 7 institutions in 3 countries.

Karo TanakaCenter for Neural Tumor Research and Section on Genetics of Hereditary Ear Disorders, House Research Institute, University of California, Los Angeles, CA 90057, USA.
Ascia Eskin
Fabrice Chareyre
Walter J Jessen
Jan Manent
Michiko Niwa-Kawakita
Ruihong Chen
Cory H White
Jeremie Vitte
Zahara M Jaffer
Stanley F Nelson
Allan E Rubenstein
Marco Giovannini
Nexgenix Pharmaceuticals (United States) · USNYU Langone Health · USCovance (United States) · USInserm · FRCentre National de la Recherche Scientifique · FRUniversité Paris Cité · FRUniversity of Southern California · US

Funding

Stem CellsP30HD004612 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 1985 to 2014
$19.5M
NICHD NIH HHS P30 HD004612
6 · The paper itself

Abstract

purposeThe growth and survival of neurofibromatosis type 2 (NF2)-deficient cells are enhanced by the activation of multiple signaling pathways including ErbBs/IGF-1R/Met, PI3K/Akt, and Ras/Raf/Mek/Erk1/2. The chaperone protein HSP90 is essential for the stabilization of these signaling molecules. The aim of the study was to characterize the effect of HSP90 inhibition in various NF2-deficient models. EXPERIMENTAL

designWe tested efficacy of the small-molecule NXD30001, which has been shown to be a potent HSP90 inhibitor. The antiproliferative activity of NXD30001 was tested in NF2-deficient cell lines and in human primary schwannoma and meningioma cultures in vitro. The antitumor efficacy of HSP90 inhibition in vivo was verified in two allograft models and in one NF2 transgenic model. The underlying molecular alteration was further characterized by a global transcriptome approach.

resultsNXD30001 induced degradation of client proteins in and suppressed proliferation of NF2-deficient cells. Differential expression analysis identified subsets of genes implicated in cell proliferation, cell survival, vascularization, and Schwann cell differentiation whose expression was altered by NXD30001 treatment. The results showed that NXD30001 in NF2-deficient schwannoma suppressed multiple pathways necessary for tumorigenesis.

conclusionsHSP90 inhibition showing significant antitumor activity against NF2-related tumor cells in vitro and in vivo represents a promising option for novel NF2 therapies.

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationFemaleHSP90 Heat-Shock ProteinsHumansLactonesMiceMice, NudeMice, TransgenicNeurofibromatosis 2OximesProteolysisTranscriptomeXenograft Model Antitumor AssaysAntineoplastic AgentsHSP90AA1 protein, humanHSP90AB1 protein, humanHSP90 Heat-Shock ProteinsLactonesOximespochoxime A

Identifiers

PMID23714726
PMCPMC4331126
OpenAlexW2158200820

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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.