Evidence map›Paper›PMID 26635611›Full record

ArticleFrontiers in pharmacology2015

Desert Hedgehog/Patch2 Axis Contributes to Vascular Permeability and Angiogenesis in Glioblastoma.

Sandy Azzi, Lucas Treps, Héloïse M Leclair, Hai-Mi Ngo, Elizabeth Harford-Wright, Julie Gavard

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Patched-2 functions to limit Patched-1 deficient skin cancer growth.Cellular oncology (Dordrecht, Netherlands) · 2018
    Article
  9. 3D Endothelial Cell Migration.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  10. Article
  11. Article
  12. Article
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 3 institutions in 1 country.

Sandy AzziINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France.
Lucas TrepsINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France.
Héloïse M LeclairINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France ; INSERM, U892, CNRS, UMR6299, Université de Nantes , Nantes, France.
Hai-Mi NgoINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France.
Elizabeth Harford-WrightINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France ; INSERM, U892, CNRS, UMR6299, Université de Nantes , Nantes, France.
Julie GavardINSERM, U1016, CNRS, UMR8104, Université Paris Descartes , Paris, France ; INSERM, U892, CNRS, UMR6299, Université de Nantes , Nantes, France.
Inserm · FRCentre National de la Recherche Scientifique · FRDélégation Paris 5 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) constitutes the most common and the most aggressive type of human tumors affecting the central nervous system. Prognosis remains dark due to the inefficiency of current treatments and the rapid relapse. Paralleling other human tumors, GBM contains a fraction of tumor initiating cells with the capacity to self-renew, initiate and maintain the tumor mass. These cells were found in close proximity to brain vasculature, suggesting functional interactions between brain tumor-initiating cells (BTICs) and endothelial cells within the so-called vascular niche. However, the mechanisms by which these cells impact on the endothelium plasticity and function remain unclear. Using culture of BTICs isolated from a cohort of 14 GBM patients, we show that BTICs secretome promotes brain endothelial cell remodeling in a VEGF-independent manner. Gene array analysis unmasked that BTICs-released factors drove the expression of Ptch2 in endothelial cells. Interestingly, BTICs produce desert hedgehog (DHH) ligand, enabling a paracrine DHH/Ptch2 signaling cascade that conveys elevated permeability and angiogenesis. Finally, DHH silencing in BTICs dramatically reduced tumor growth, as well as vascularization and intra-tumor permeability. Collectively, our data unveil a role for DHH in exacerbated tumor angiogenesis and permeability, which may ultimately favor glioblastoma growth, and thus place the DHH/Ptch2 nexus as a molecular target for novel therapies.

Indexed as

brain endothelial cellsgliomahedgehogpermeabilitytumor vasculature

Identifiers

PMID26635611
PMCPMC4657436
OpenAlexW2180305554

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.