Evidence map›Paper›PMID 21305617›Full record

ReviewGlia2011

Genetic modeling of gliomas in mice: new tools to tackle old problems.

Dolores Hambardzumyan, Luis F Parada, Eric C Holland, Al Charest

Open access · greenAbstract readReview
In one paragraph

Review in Glia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. A clinically relevant model and method to study necrosis as a driving force in glioma restructuring and progression.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024
    Review
  8. Article
  9. Review
  10. Translational Models in Glioma Immunotherapy Research.Current oncology (Toronto, Ont.) · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

5 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

4 authors at 4 institutions in 2 countries.

Dolores HambardzumyanDepartment of Stem Cell Biology and Regenerative Medicine, Cleveland Clinic, Ohio, USA. hambard@ccf.org
Luis F Parada
Eric C Holland
Al Charest
Cleveland Clinic · USMemorial Sloan Kettering Cancer Center · USThe University of Texas Southwestern Medical Center · USTufts University · US

Funding

Understanding and Eliminating Oncogenic EGFR Signaling in Malignant GliomaU01CA141556 · NCI · TUFTS MEDICAL CENTER · PI CHAREST, ALAIN · 2009 to 2013
$3.3M
Genetic Mouse Models of GliomaR01CA131313 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PARADA, LUIS FERNANDO · 2009 to 2016
$3.2M
NCI NIH HHS R01 CA131313NCI NIH HHS U01 CA141556
6 · The paper itself

Abstract

The recently published comprehensive profiles of genomic alterations in glioma have led to a refinement in our understanding of the molecular events that underlie this cancer. Using state-of-the-art genomic tools, several laboratories have created and characterized accurate genetically engineered mouse models of glioma based on specific genetic alterations observed in human tumors. These in vivo brain tumor models faithfully recapitulate the histopathology, etiology, and biology of gliomas and provide an exceptional experimental system to discover novel therapeutic targets and test therapeutic agents. This review focuses on mouse models of glioma with a special emphasis on genetically engineered models developed around key genetic glioma signature mutations in the PDGFR, EGFR, and NF1 genes and pathways. The resulting animal models have provided insight into many fundamental and mechanistic facets of tumor initiation, maintenance and resistance to therapeutic intervention and will continue to do so in the future.

Indexed as

Disease Models, AnimalAnimalsBrain NeoplasmsErbB ReceptorsGliomaHumansMiceMice, TransgenicMutationNeurofibromin 1Platelet-Derived Growth FactorSignal TransductionErbB ReceptorsNeurofibromin 1Platelet-Derived Growth Factor

Identifiers

PMID21305617
PMCPMC3619979
OpenAlexW2108854209

What OpenQuestion holds

Textmetadata
LicenceTDM
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.