Evidence map›Paper›PMID 24809734›Full record

ArticleOncotarget2014

Anti-vascular endothelial growth factor therapy-induced glioma invasion is associated with accumulation of Tie2-expressing monocytes.

Konrad Gabrusiewicz, Dan Liu, Nahir Cortes-Santiago, Mohammad B Hossain, Charles A Conrad, Kenneth D Aldape, Gregory N Fuller, Frank C Marini, Marta M Alonso, Miguel Angel Idoate and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 81 citations in OpenAlex.

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  13. Adaptor Protein ShcD/Molecular cancer research : MCR · 2021
    Article
  14. Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.International journal of molecular sciences · 2021
    Review
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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 3 institutions in 2 countries.

Konrad GabrusiewiczDepartment of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Dan Liu
Nahir Cortes-Santiago
Mohammad B Hossain
Charles A Conrad
Kenneth D Aldape
Gregory N Fuller
Frank C Marini
Marta M Alonso
Miguel Angel Idoate
Mark R Gilbert
Juan Fueyo
Candelaria Gomez-Manzano
The University of Texas MD Anderson Cancer Center · USUniversidad de Navarra · ESWake Forest University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Role of TEMs in brain tumor dispersalR01NS069964 · NINDS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GOMEZ-MANZANO, CANDELARIA, MARINI, FRANK C. · 2010 to 2014
$1.7M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NINDS NIH HHS R01 NS069964
6 · The paper itself

Abstract

The addition of anti-angiogenic therapy to the few treatments available to patients with malignant gliomas was based on the fact that these tumors are highly vascularized and on encouraging results from preclinical and clinical studies. However, tumors that initially respond to this therapy invariably recur with the acquisition of a highly aggressive and invasive phenotype. Although several myeloid populations have been associated to this pattern of recurrence, a specific targetable population has not been yet identified. Here, we present evidence for the accumulation of Tie2-expressing monocytes/macrophages (TEMs) at the tumor/normal brain interface of mice treated with anti-VEGF therapies in regions with heightened tumoral invasion. Furthermore, we describe the presence of TEMs in malignant glioma surgical specimens that recurred after bevacizumab treatment. Our studies showed that TEMs enhanced the invasive properties of glioma cells and secreted high levels of gelatinase enzymatic proteins. Accordingly, Tie2⁺MMP9⁺ monocytic cells were consistently detected in the invasive tumor edge upon anti-VEGF therapies. Our results suggest the presence of a specific myeloid/monocytic subpopulation that plays a pivotal role in the mechanism of escape of malignant gliomas from anti-VEGF therapies and therefore constitutes a new cellular target for combination therapies in patients selected for anti-angiogenesis treatment.

Indexed as

Angiogenesis InhibitorsAnimalsAntibodies, Monoclonal, HumanizedBevacizumabBrain NeoplasmsDrug Resistance, NeoplasmEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueGliomaHumansImmunohistochemistryMatrix Metalloproteinase 9MiceMice, NudeMicroscopy, ConfocalAngiogenesis InhibitorsAntibodies, Monoclonal, HumanizedBevacizumabMatrix Metalloproteinase 9Receptor, TIE-2Vascular Endothelial Growth Factor A

Identifiers

PMID24809734
PMCPMC4039157
OpenAlexW1556310643

What OpenQuestion holds

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LicenceCC BY
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.