Evidence map›Paper›PMID 28035003›Full record

ArticleThe Journal of biological chemistry2017

A Quininib Analogue and Cysteinyl Leukotriene Receptor Antagonist Inhibits Vascular Endothelial Growth Factor (VEGF)-independent Angiogenesis and Exerts an Additive Antiangiogenic Response with Bevacizumab.

Clare T Butler, Alison L Reynolds, Miriam Tosetto, Eugene T Dillon, Patrick J Guiry, Gerard Cagney, Jacintha O'Sullivan, Breandán N Kennedy

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Investigating the antiangiogenic potential ofSaudi journal of biological sciences · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Identification of mundoserone by zebrafishExperimental and therapeutic medicine · 2018
    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

8 authors at 3 institutions in 1 country.

Clare T ButlerFrom the UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and.
Alison L ReynoldsFrom the UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and.
Miriam TosettoCentre for Colorectal Disease, St. Vincent's University Hospital, Dublin 4, Ireland, and.
Eugene T DillonFrom the UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and.
Patrick J GuiryUCD School of Chemistry, UCD Centre for Synthesis and Chemical Biology, University College Dublin, Belfield, Dublin 4, Ireland.
Gerard CagneyFrom the UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and.
Jacintha O'SullivanTrinity Translational Medicine Institute, Department of Surgery, Trinity College Dublin, St. James's Hospital, Dublin 8, Ireland.
Breandán N KennedyFrom the UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and brendan.kennedy@ucd.ie.
University College Dublin · IESt. Vincent's University Hospital · IETrinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess blood vessel growth contributes to the pathology of metastatic cancers and age-related retinopathies. Despite development of improved treatments, these conditions are associated with high economic costs and drug resistance. Bevacizumab (Avastin®), a monoclonal antibody against vascular endothelial growth factor (VEGF), is used clinically to treat certain types of metastatic cancers. Unfortunately, many patients do not respond or inevitably become resistant to bevacizumab, highlighting the need for more effective antiangiogenic drugs with novel mechanisms of action. Previous studies discovered quininib, an antiangiogenic small molecule antagonist of cysteinyl leukotriene receptors 1 and 2 (CysLT

Indexed as

Angiogenesis InhibitorsAnimalsAnimals, Genetically ModifiedBenzene DerivativesBevacizumabCell LineCell MovementCell SurvivalCysteineDose-Response Relationship, DrugEndothelial CellsGreen Fluorescent ProteinsHumansLeukotriene AntagonistsMicroscopy, FluorescenceNeovascularization, PathologicAngiogenesis InhibitorsBenzene DerivativesBevacizumabCysteineGreen Fluorescent ProteinsLeukotriene AntagonistsPhenolsquininibQuinolinesRecombinant ProteinsVascular Endothelial Growth Factor Aangiogenesiscalpaincell migrationcolorectal cancerdrug developmentendothelial cellG protein-coupled receptor (GPCR)leukotrienepharmacologyvascular endothelial growth factor (VEGF)

Identifiers

PMID28035003
PMCPMC5339742
OpenAlexW2565670405

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.