Evidence map›Paper›PMID 25851538›Full record

ArticleEMBO molecular medicine2015

Vasculotide reduces endothelial permeability and tumor cell extravasation in the absence of binding to or agonistic activation of Tie2.

Florence T H Wu, Christina R Lee, Elena Bogdanovic, Aaron Prodeus, Jean Gariépy, Robert S Kerbel

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

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  17. Pharmacological Tie2 activation in kidney transplantation.World journal of transplantation · 2016
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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

6 authors at 3 institutions in 1 country.

Florence T H WuDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.
Christina R LeeBiological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.
Elena BogdanovicBiological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.
Aaron ProdeusDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada Physical Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.
Jean GariépyDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada Physical Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada.
Robert S KerbelDepartment of Medical Biophysics, University of Toronto, Toronto, ON, Canada Biological Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada robert.kerbel@sri.utoronto.ca.
Sunnybrook Research InstituteSunnybrook Health Science Centre · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiopoietin-1 (Ang1) activation of Tie2 receptors on endothelial cells (ECs) reduces adhesion by tumor cells (TCs) and limits junctional permeability to TC diapedesis. We hypothesized that systemic therapy with Vasculotide (VT)-a purported Ang1 mimetic, Tie2 agonist-can reduce the extravasation of potentially metastatic circulating TCs by similarly stabilizing the host vasculature. In vitro, VT and Ang1 treatments impeded endothelial hypermeability and the transendothelial migration of MDA-MB-231∙LM2-4 (breast), HT29 (colon), or SN12 (renal) cancer cells to varying degrees. In mice, VT treatment inhibited the transit of TCs through the pulmonary endothelium, but not the hepatic or lymphatic endothelium. In the in vivo LM2-4 model, VT monotherapy had no effect on primary tumors, but significantly delayed distant metastatic dissemination to the lungs. In the post-surgical adjuvant treatment setting, VT therapeutically complemented sunitinib therapy, an anti-angiogenic tyrosine kinase inhibitor which limited the local growth of residual disease. Unexpectedly, detailed investigations into the putative mechanism of action of VT revealed no evidence of Tie2 agonism or Tie2 binding; alternative mechanisms have yet to be determined.

Indexed as

Angiopoietin-1AnimalsBreast NeoplasmsCell Line, TumorEndothelial CellsMiceNeoplasm MetastasisPermeabilityReceptor, TIE-2Transendothelial and Transepithelial MigrationAngiopoietin-1Angpt1 protein, mouseReceptor, TIE-2Tek protein, mouseangiopoietinmetastasisTie2tumor cell extravasationvascular permeability

Identifiers

PMID25851538
PMCPMC4459817
OpenAlexW2135398396

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.