Evidence map›Paper›PMID 27655684›Full record

ArticleOncotarget2016

Antitumor activity of a novel anti-vascular endothelial growth factor receptor-1 monoclonal antibody that does not interfere with ligand binding.

Grazia Graziani, Federica Ruffini, Lucio Tentori, Manuel Scimeca, Annalisa S Dorio, Maria Grazia Atzori, Cristina M Failla, Veronica Morea, Elena Bonanno, Stefania D'Atri and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 45 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Grazia GrazianiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Federica RuffiniLaboratory of Molecular Oncology, "Istituto Dermopatico dell'Immacolata"-IRCCS, Rome, Italy.
Lucio TentoriDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Manuel ScimecaDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Annalisa S DorioDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Maria Grazia AtzoriDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
Cristina M FaillaLaboratory of Experimental Immunology, "Istituto Dermopatico dell'Immacolata"-IRCCS, Rome, Italy.
Veronica MoreaNational Research Council of Italy (CNR), Institute of Molecular Biology and Pathology, Rome, Italy.
Elena BonannoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Stefania D'AtriLaboratory of Molecular Oncology, "Istituto Dermopatico dell'Immacolata"-IRCCS, Rome, Italy.
Pedro M LacalLaboratory of Molecular Oncology, "Istituto Dermopatico dell'Immacolata"-IRCCS, Rome, Italy.
University of Rome Tor Vergata · ITIstituto Dermopatico dell'Immacolata · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor receptor-1 (VEGFR-1) is a tyrosine kinase transmembrane receptor that has also a soluble isoform containing most of the extracellular ligand binding domain (sVEGFR-1). VEGF-A binds to both VEGFR-2 and VEGFR-1, whereas placenta growth factor (PlGF) interacts exclusively with VEGFR-1. In this study we generated an anti-VEGFR-1 mAb (D16F7) by immunizing BALB/C mice with a peptide that we had previously reported to inhibit angiogenesis and endothelial cell migration induced by PlGF. D16F7 did not affect binding of VEGF-A or PlGF to VEGFR-1, thus allowing sVEGFR-1 to act as decoy receptor for these growth factors, but it hampered receptor homodimerization and activation. D16F7 inhibited both the chemotactic response of human endothelial, myelomonocytic and melanoma cells to VEGFR-1 ligands and vasculogenic mimicry by tumor cells. Moreover, D16F7 exerted in vivo antiangiogenic effects in a matrigel plug assay. Importantly, D16F7 inhibited tumor growth and was well tolerated by B6D2F1 mice injected with syngeneic B16F10 melanoma cells. The antitumor effect was associated with melanoma cell apoptosis, vascular abnormalities and decrease of both monocyte/macrophage infiltration and myeloid progenitor mobilization. For all the above, D16F7 may be exploited in the therapy of metastatic melanoma and other tumors or pathological conditions involving VEGFR-1 activation.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic Agents, ImmunologicalCell Line, TumorCell MovementDisease Models, AnimalFemaleHematopoietic Stem CellsHumansHuman Umbilical Vein Endothelial CellsLigandsMacrophagesMaleMelanoma, ExperimentalMembrane ProteinsMiceAngiogenesis InhibitorsAntineoplastic Agents, ImmunologicalLigandsMembrane ProteinsPIGF protein, humanVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1angiogenesismelanomamonocyte/macrophagePlGFVEGFR-1

Identifiers

PMID27655684
PMCPMC5341950
OpenAlexW2522288290

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.