Evidence map›Paper›PMID 27262114›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2016

Molecular Pathways: Endothelial Cell FAK-A Target for Cancer Treatment.

Marina Roy-Luzarraga, Kairbaan Hodivala-Dilke

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 99 citations in OpenAlex.

  1. Endothelial Cell pY397-FAK Expression Predicts the Risk of Breast Cancer Recurrences after Radiotherapy in the SweBCG91-RT Cohort.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  19. Linc00662 mAmerican journal of cancer research · 2023
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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

2 authors at 1 institution in 1 country.

Marina Roy-LuzarragaAdhesion and Angiogenesis Laboratory, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Kairbaan Hodivala-DilkeAdhesion and Angiogenesis Laboratory, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom. k.hodivala-dilke@qmul.ac.uk.
Queen Mary University of London · GB

Funding

Cancer Research UK 12007Cancer Research UK 18673Cancer Research UK C8218/A18673Cancer Research UK C8218/A21453Medical Research Council G0901609Worldwide Cancer Research 12-1068
6 · The paper itself

Abstract

The nonreceptor protein tyrosine kinase, focal adhesion kinase (FAK, also known as PTK2), is a key mediator of signal transduction downstream of integrins and growth factor receptors in a variety of cells, including endothelial cells. FAK is upregulated in several advanced-stage solid tumors and has been described to promote tumor progression and metastasis through effects on both tumor cells and stromal cells. This observation has led to the development of several FAK inhibitors, some of which have entered clinical trials (GSK2256098, VS-4718, VS-6062, VS-6063, and BI853520). Resistance to chemotherapy is a serious limitation of cancer treatment and, until recently, most studies were restricted to tumor cells, excluding the possible roles performed by the tumor microenvironment. A recent report identified endothelial cell FAK (EC-FAK) as a major regulator of chemosensitivity. By dysregulating endothelial cell-derived paracrine (also known as angiocrine) signals, loss of FAK solely in the endothelial cell compartment is able to induce chemosensitization to DNA-damaging therapies in the malignant cell compartment and thereby reduce tumor growth. Herein, we summarize the roles of EC-FAK in cancer and development and review the status of FAK-targeting anticancer strategies. Clin Cancer Res; 22(15); 3718-24. ©2016 AACR.

Indexed as

AnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsClinical Trials as TopicDrug Resistance, NeoplasmEndothelial CellsFocal Adhesion Protein-Tyrosine KinasesHumansNeoplasmsProtein Kinase InhibitorsSignal TransductionTreatment OutcomeAntineoplastic AgentsFocal Adhesion Protein-Tyrosine KinasesProtein Kinase Inhibitors

Identifiers

PMID27262114
PMCPMC5386133
OpenAlexW2414519095

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.