Evidence map›Paper›PMID 22858156›Full record

ReviewThe American journal of pathology2012

Mechanisms of glioma-associated neovascularization.

Matthew E Hardee, David Zagzag

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
248citing papers in PubMed, 3 pooled it
9.0field-weighted citation impact, top 1% 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

248 citing papers in PubMed, 3 syntheses or guidelines pooled it, 462 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Physiologic MR imaging of the tumor microenvironment revealed switching of metabolic phenotype upon recurrence of glioblastoma in humans.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Trial
  5. The prognostic value of [European journal of nuclear medicine and molecular imaging · 2018
    Trial
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  8. Biomimetic Scaffold-Based 3D Models for Decoding Cancer Biology and Advancing Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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188 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

2 authors at 1 institution in 1 country.

Matthew E HardeeDepartment of Radiation Oncology, New York University School of Medicine, New York, New York 10016, USA.
David Zagzag
New York University · US

Funding

Invasion and Angiogenesis in Malignant GliomasR01CA100426 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZAGZAG, DAVID · 2004 to 2008
$1.4M
Novel CXCR4 Therapeutics to Block Bevacizumab-Induced Glioma Dissemination.R21NS074055 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ZAGZAG, DAVID · 2011 to 2013
$570k
NCI NIH HHS R01-CA100426-0141NINDS NIH HHS 1R21-NS074055-01A1NINDS NIH HHS R21 NS074055
6 · The paper itself

Abstract

Glioblastomas (GBMs), the most common primary brain tumor in adults, are characterized by resistance to chemotherapy and radiotherapy. One of the defining characteristics of GBM is an abundant and aberrant vasculature. The processes of vascular co-option, angiogenesis, and vasculogenesis in gliomas have been extensively described. Recently, however, it has become clear that these three processes are not the only mechanisms by which neovascularization occurs in gliomas. Furthermore, it seems that these processes interact extensively, with potential overlap among them. At least five mechanisms by which gliomas achieve neovascularization have been described: vascular co-option, angiogenesis, vasculogenesis, vascular mimicry, and (the most recently described) glioblastoma-endothelial cell transdifferentiation. We review these mechanisms in glioma neovascularization, with a particular emphasis on the roles of hypoxia and glioma stem cells in each process. Although some of these processes are well established, others have been identified only recently and will need to be further investigated for complete validation. We also review strategies to target glioma neovascularization and the development of resistance to these therapeutic strategies. Finally, we describe how these complex processes interlink and overlap. A thorough understanding of the contributing molecular processes that control the five modalities reviewed here should help resolve the treatment resistance that characterizes GBMs.

Indexed as

Angiogenesis InhibitorsAnimalsBrain NeoplasmsCell HypoxiaGliomaHumansNeoplastic Stem CellsNeovascularization, PathologicAngiogenesis Inhibitors

Identifiers

PMID22858156
PMCPMC3463636
OpenAlexW2041532314

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.