Evidence map›Paper›PMID 28444899›Full record

ArticleThe Journal of pathology2017

Focal Adhesion Kinase (FAK) tyrosine 397E mutation restores the vascular leakage defect in endothelium-specific FAK-kinase dead mice.

Annika N Alexopoulou, Delphine M Lees, Natalia Bodrug, Tanguy Lechertier, Isabelle Fernandez, Gabriela D'Amico, Matthew Dukinfield, Silvia Batista, Bernardo Tavora, Bryan Serrels and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2017. 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
1.7field-weighted citation impact, top 17% 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, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The roles of nuclear focal adhesion kinase (FAK) on Cancer: a focused review.Journal of experimental & clinical cancer research : CR · 2019
    Review
  11. Article
  12. Review
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 5 institutions in 3 countries.

Annika N AlexopoulouDepartment of Molecular Oncology, BSRC Alexander Fleming, Athens, Greece.ORCID 0000-0001-9404-8133
Delphine M LeesCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-2119-3978
Natalia BodrugCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Tanguy LechertierCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Isabelle FernandezPlatform of Expertise for Rare Diseases Paris-Sud, Le Kremlin-Bicêtre, France.
Gabriela D'AmicoCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Matthew DukinfieldCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Silvia BatistaDivision of Cancer Therapeutics, Institute of Cancer Research, Sutton, UK.
Bernardo TavoraLaboratory of Systems Cancer Biology, Rockefeller University, New York, USA.
Bryan SerrelsCancer Research UK Edinburgh Centre, University of Edinburgh, Edinburgh, UK.
Kairbaan Hodivala-DilkeCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Queen Mary University of London · GBAlexander Fleming Biomedical Sciences Research Center · GREdinburgh Cancer Research · GBInstitute of Cancer Research · GBRockefeller University · US

Funding

Cancer Research UK 12007Cancer Research UK 18673Cancer Research UK 8218/A18673
6 · The paper itself

Abstract

Focal adhesion kinase (FAK) inhibitors have been developed as potential anticancer agents and are undergoing clinical trials. In vitro activation of the FAK kinase domain triggers autophosphorylation of Y397, Src activation, and subsequent phosphorylation of other FAK tyrosine residues. However, how FAK Y397 mutations affect FAK kinase-dead (KD) phenotypes in tumour angiogenesis in vivo is unknown. We developed three Pdgfb-iCre

Indexed as

AnimalsAntineoplastic Agents, HormonalCapillary PermeabilityCell DivisionCell HypoxiaCell Line, TumorEndothelium, VascularFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHomozygoteMelanomaMiceMutationNeoplasm TransplantationNeovascularization, PathologicTamoxifenAntineoplastic Agents, HormonalFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesPtk2 protein, mouseTamoxifenfocal adhesion kinasetumour angiogenesis

Identifiers

PMID28444899
PMCPMC5518444
OpenAlexW2623861266

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.