Evidence map›Paper›PMID 22179835›Full record

ArticleOncogene2012

Mer receptor tyrosine kinase inhibition impedes glioblastoma multiforme migration and alters cellular morphology.

A E J Rogers, J P Le, S Sather, B M Pernu, D K Graham, A M Pierce, A K Keating

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. MERTK Inhibition as a Targeted Novel Cancer Therapy.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Immuno-oncology: are TAM receptors in glioblastoma friends or foes?Cell communication and signaling : CCS · 2021
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

7 authors at 2 institutions in 1 country.

A E J RogersDepartment of Pediatrics, University of Colorado School of Medicine, and Department of Pediatrics, Children's Hospital Colorado, Aurora, CO 80045, USA.
J P Le
S Sather
B M Pernu
D K Graham
A M Pierce
A K Keating
University of Colorado Denver · USChildren's Hospital Colorado · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
POSTGRADUATE TRAINING IN PEDIATRIC ONCOLOGYT32CA082086 · NCI · UNIVERSITY OF COLORADO DENVER · PI GORE, LIA · 2000 to 2015
$4.1M
Training in Basic and Translational Child Health ResearchK12HD068372 · NICHD · UNIVERSITY OF COLORADO DENVER · PI DANIELS, STEPHEN R · 2011 to 2020
$3.7M
Novel Biologically Targeted Therapy Against the Mer and Axl Receptor Tyrosine KinR01CA137078 · NCI · UNIVERSITY OF COLORADO DENVER · PI GRAHAM, DOUGLAS K · 2010 to 2014
$1.5M
NCI NIH HHS P30 CA046934NCI NIH HHS R01 1CA137078NCI NIH HHS R01 CA137078NCI NIH HHS T32 CA082086NICHD NIH HHS K12 HD068372
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is an aggressive brain tumor, fatal within 1 year from diagnosis in most patients despite intensive multimodality therapy. The migratory and microscopically invasive nature of GBM as well as its resistance to chemotherapy renders conventional therapies inadequate in its treatment. Although Mer receptor tyrosine kinase (RTK) inhibition has been shown to decrease the long-term survival and improve the chemosensitivity of GBM in vitro, its role in malignant cellular migration has not been previously evaluated. In this study, we report for the first time a role for Mer RTK in brain tumor migration and show that Mer inhibition profoundly impedes GBM migration and alters cellular morphology. Our data demonstrate that Mer RTK inhibition results in altered signaling through focal adhesion kinase (FAK) and RhoA GTPase and a transformation of cytoskeletal organization, suggesting both molecular and structural mechanisms for the abrogation of migration. We also describe a novel and translational method of Mer RTK inhibition using a newly developed monoclonal antibody, providing proof of principle for future evaluation of Mer-targeted translational therapies in the treatment of GBM. Previous findings implicating Mer signaling in glioblastoma survival and chemotherapy resistance coupled with our discovery of the role of Mer RTK in GBM cellular migration support the development of novel Mer-targeted therapies for this devastating disease.

Indexed as

AnimalsAntibodies, MonoclonalCell Line, TumorCell Movementc-Mer Tyrosine KinaseEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesGene ExpressionGlioblastomaHumansMiceProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesrhoA GTP-Binding ProteinRNA InterferenceSignal TransductionAntibodies, Monoclonalc-Mer Tyrosine KinaseFocal Adhesion Protein-Tyrosine KinasesMERTK protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesrhoA GTP-Binding Protein

Identifiers

PMID22179835
PMCPMC3939856
OpenAlexW2016660437

What OpenQuestion holds

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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.