Evidence map›Paper›PMID 15831232›Full record

ReviewNeuro-oncology2005

Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis.

Balveen Kaur, Fatima W Khwaja, Eric A Severson, Shannon L Matheny, Daniel J Brat, Erwin G Van Meir

Open access · greenAbstract readReview
In one paragraph

Review in Neuro-oncology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 371 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
371citing papers in PubMed, 3 pooled it
7.8field-weighted citation impact, top 2% 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

371 citing papers in PubMed, 3 syntheses or guidelines pooled it, 682 citations in OpenAlex.

  1. Pooled it
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  4. Phase II Investigation of TVB-2640 (Denifanstat) with Bevacizumab in Patients with First Relapse High-Grade Astrocytoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Trial
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311 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

6 authors at 1 institution in 1 country.

Balveen KaurLaboratory of Molecular Neuro-Oncology, Department of Neurosurgery and Hematology/Oncology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Fatima W Khwaja
Eric A Severson
Shannon L Matheny
Daniel J Brat
Erwin G Van Meir
Emory University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
THERAPEUTIC MODULATION OF ANGIOGENESIS IN HUMAN GLIOMASR01CA086335 · NCI · EMORY UNIVERSITY · PI VAN MEIR, ERWIN G. · 2000 to 2011
$3.9M
A hypoxia-dependent adenovirus for glioma therapyR01CA087830 · NCI · EMORY UNIVERSITY · PI VAN MEIR, ERWIN G · 2002 to 2005
$1.3M
NCI NIH HHS CA 86335NCI NIH HHS CA 87830NCI NIH HHS R01 CA086335NCI NIH HHS R01 CA087830NIGMS NIH HHS T32 GM008169NINDS NIH HHS NS 42943
6 · The paper itself

Abstract

Glioblastomas, like other solid tumors, have extensive areas of hypoxia and necrosis. The importance of hypoxia in driving tumor growth is receiving increased attention. Hypoxia-inducible factor 1 (HIF-1) is one of the master regulators that orchestrate the cellular responses to hypoxia. It is a heterodimeric transcription factor composed of alpha and beta subunits. The alpha subunit is stable in hypoxic conditions but is rapidly degraded in normoxia. The function of HIF-1 is also modulated by several molecular mechanisms that regulate its synthesis, degradation, and transcriptional activity. Upon stabilization or activation, HIF-1 translocates to the nucleus and induces transcription of its downstream target genes. Most important to gliomagenesis, HIF-1 is a potent activator of angiogenesis and invasion through its upregulation of target genes critical for these functions. Activation of the HIF-1 pathway is a common feature of gliomas and may explain the intense vascular hyperplasia often seen in glioblastoma multiforme. Activation of HIF results in the activation of vascular endothelial growth factors, vascular endothelial growth factor receptors, matrix metalloproteinases, plasminogen activator inhibitor, transforming growth factors alpha and beta, angiopoietin and Tie receptors, endothelin-1, inducible nitric oxide synthase, adrenomedullin, and erythropoietin, which all affect glioma angiogenesis. In conclusion, HIF is a critical regulatory factor in the tumor microenvironment because of its central role in promoting proangiogenic and invasive properties. While HIF activation strongly promotes angiogenesis, the emerging vasculature is often abnormal, leading to a vicious cycle that causes further hypoxia and HIF upregulation.

Indexed as

DNA-Binding ProteinsNuclear ProteinsTranscription FactorsBrain NeoplasmsGliomaHumansHypoxiaHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitNeovascularization, PathologicSignal TransductionDNA-Binding ProteinsHIF1A protein, humanHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitNuclear ProteinsTranscription Factors

Identifiers

PMID15831232
PMCPMC1871894
OpenAlexW1988692970

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.