Evidence map›Paper›PMID 31784455›Full record

ArticleMolecular cancer therapeutics2020

A Synergistic Anticancer FAK and HDAC Inhibitor Combination Discovered by a Novel Chemical-Genetic High-Content Phenotypic Screen.

John C Dawson, Bryan Serrels, Adam Byron, Morwenna T Muir, Ashraff Makda, Amaya García-Muñoz, Alex von Kriegsheim, Daniel Lietha, Neil O Carragher, Margaret C Frame

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2020. 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
0.9field-weighted citation impact, top 25% 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, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  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

10 authors at 3 institutions in 3 countries.

John C Dawson *Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
Bryan Serrels *Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
Adam Byron *Cancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0002-5939-9883
Morwenna T MuirCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.ORCID 0000-0001-5835-3886
Ashraff MakdaCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
Amaya García-MuñozSystems Biology Ireland, University College Dublin, Dublin, Ireland.
Alex von KriegsheimCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
Daniel LiethaCell Signaling and Adhesion Group, Structural Biology Program, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Neil O CarragherCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom. m.frame@ed.ac.uk n.carragher@ed.ac.uk.
Margaret C FrameCancer Research UK Edinburgh Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom. m.frame@ed.ac.uk n.carragher@ed.ac.uk.
Edinburgh Cancer Research · GBUniversity College Dublin · IESpanish National Cancer Research Centre · ES

Funding

Cancer Research UK 15703Cancer Research UK 24837Cancer Research UK A15703Cancer Research UK C157/A15703Cancer Research UK C157/A24837European Research Council 294440
6 · The paper itself

Abstract

We mutated the focal adhesion kinase (FAK) catalytic domain to inhibit binding of the chaperone Cdc37 and ATP, mimicking the actions of a FAK kinase inhibitor. We reexpressed mutant and wild-type FAK in squamous cell carcinoma (SCC) cells from which endogenous FAK had been deleted, genetically fixing one axis of a FAK inhibitor combination high-content phenotypic screen to discover drugs that may synergize with FAK inhibitors. Histone deacetylase (HDAC) inhibitors represented the major class of compounds that potently induced multiparametric phenotypic changes when FAK was rendered kinase-defective or inhibited pharmacologically in SCC cells. Combined FAK and HDAC inhibitors arrest proliferation and induce apoptosis in a subset of cancer cell lines

Indexed as

AnimalsCell ProliferationDrug SynergismFocal Adhesion Protein-Tyrosine KinasesHistone Deacetylase InhibitorsHumansMiceNeoplasmsSignal TransductionFocal Adhesion Protein-Tyrosine KinasesHistone Deacetylase Inhibitors

Identifiers

PMID31784455
PMCPMC7611632
OpenAlexW2989718988

What OpenQuestion holds

Textmetadata
LicenceTDM
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.