ArticleCancer letters2014
Targeting the C-terminal focal adhesion kinase scaffold in pancreatic cancer.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Design, synthesis, and biological evaluation of potent FAK-degrading PROTACs.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Design, Synthesis, and Evaluation of Highly Potent FAK-Targeting PROTACs.ACS medicinal chemistry letters · 2020Article
- Neutrophil-mimicking therapeutic nanoparticles for targeted chemotherapy of pancreatic carcinoma.Acta pharmaceutica Sinica. B · 2019Article
- Review
- Subgroup analysis reveals molecular heterogeneity and provides potential precise treatment for pancreatic cancers.OncoTargets and therapy · 2018Article
- The extracellular matrix and focal adhesion kinase signaling regulate cancer stem cell function in pancreatic ductal adenocarcinoma.PloS one · 2017Article
- PROTACs: great opportunities for academia and industry.Signal transduction and targeted therapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Preliminary studies in our laboratory have demonstrated the importance of both the NH2 and COOH terminus scaffolding functions of focal adhesion kinase (FAK). Here, we describe a new small molecule inhibitor, C10, that targets the FAK C-terminus scaffold. C10 showed marked selectivity for cells overexpressing VEGFR3 when tested in isogenic cell lines, MCF7 and MCF7-VEGFR3. C10 preferentially inhibited pancreatic tumor growth in vivo in cells with high FAK-Y925 and VEGFR3 expression. Treatment with C10 led to a significant inhibition in endothelial cell proliferation and tumor endothelial and lymphatic vessel density and decrease in interstitial fluid pressure. These results highlight the underlying importance of targeting the FAK scaffold to treat human cancers.
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What OpenQuestion holds
Registered trials
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.