Evidence map›Paper›PMID 25948774›Full record

ArticleOncotarget2015

Sunitinib but not VEGF blockade inhibits cancer stem cell endothelial differentiation.

Alessia Brossa, Cristina Grange, Letizia Mancuso, Laura Annaratone, Maria Antonietta Satolli, Massimiliano Mazzone, Giovanni Camussi, Benedetta Bussolati

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  8. A Review of Phosphocreatine 3 Kinase δ Subtype (PI3Kδ) and Its Inhibitors in Malignancy.Medical science monitor : international medical journal of experimental and clinical research · 2021
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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

8 authors at 2 institutions in 2 countries.

Alessia BrossaDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
Cristina GrangeDepartment of Medical Sciences, University of Torino, Torino, Italy.
Letizia MancusoDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
Laura AnnaratoneDepartment of Medical Sciences, University of Torino, Torino, Italy.
Maria Antonietta SatolliDepartment of Oncology, University of Torino, Torino, Italy.
Massimiliano MazzoneLaboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, KU Leuven, Leuven, Belgium.
Giovanni CamussiDepartment of Medical Sciences, University of Torino, Torino, Italy.
Benedetta BussolatiDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
University of Turin · ITKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different mechanisms of angiogenesis and vasculogenesis are involved in the development of the tumor vasculature. Among them, cancer stem cells are known to contribute to tumor vasculogenesis through their direct endothelial differentiation. Here, we investigated the effect of anti-angiogenic therapy on vasculogenesis of cancer stem cells derived from breast and renal carcinomas. We found that all the anti-angiogenic approaches impaired proliferation and survival of cancer stem cells once differentiated into endothelial cells in vitro and reduced murine angiogenesis in vivo. At variance, only VEGF-receptor inhibition using the non-specific tyrosine kinase inhibitor Sunitinib or the anti-VEGF-receptor 2 neutralizing antibody, but not VEGF blockade using Bevacizumab, impaired the process of endothelial differentiation in vitro, suggesting a VEGF-independent mechanism. In addition, tyrosine kinase inhibition by Sunitinib but not VEGF blockade using the soluble VEGF trap sFlk1 inhibited the cancer stem cell-induced vasculogenesis in vivo. Accordingly, Sunitinib but not Bevacizumab inhibited the induction of hypoxia-inducible factor pathway occurring during endothelial differentiation under hypoxia. The present results highlight a differential effect of VEGF-receptor blockade versus VEGF inhibition in tumor vascularization. VEGFR blockade inhibits the process of tumor vasculogenesis occurring during tumor hypoxia whereas the effect of VEGF inhibition appears restricted to differentiated endothelial cells.

Indexed as

Angiogenesis InhibitorsAnimalsBasic Helix-Loop-Helix ProteinsBevacizumabCell DifferentiationCell HypoxiaCell ProliferationCells, CulturedCell SurvivalEndothelial PAS Domain-Containing Protein 1Endothelial Progenitor CellsHumansHypoxia-Inducible Factor 1, alpha SubunitIndolesMice, SCIDNeoplastic Stem CellsAngiogenesis InhibitorsBasic Helix-Loop-Helix ProteinsBevacizumabEndothelial PAS Domain-Containing Protein 1HIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIndolesProtein Kinase InhibitorsPyrrolesSunitinibVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, humanangiogenesisangiogenic therapyHIFtumor stem cellsVEGF

Identifiers

PMID25948774
PMCPMC4484457
OpenAlexW2157000170

What OpenQuestion holds

Textmetadata
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.