ReviewScience signaling2013
Disrupting the scaffold to improve focal adhesion kinase-targeted cancer therapeutics.
Review in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed.
- Establishing selectivity of FAK-paxillin PPI inhibitor using pulldown proteomics and a focal adhesion protein selectivity panel.Biochemistry and biophysics reports · 2026Article
- Targeting the hydrophobic pockets of FAK/PYK2 FAT domain: a highly effective inhibitory strategy suppressing tumor growth and eliminating metastasis.Cell communication and signaling : CCS · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Structure-based discovery of hydrocarbon-stapled paxillin peptides that block FAK scaffolding in cancer.Nature communications · 2025Article
- Focal adhesion kinase plays an essential role in Th17 cell differentiation by stimulating NF-κB signaling.Frontiers in immunology · 2025Article
- PROTAC'ing oncoproteins: targeted protein degradation for cancer therapy.Molecular cancer · 2023Review
- The Journey of Cancer Cells to the Brain: Challenges and Opportunities.International journal of molecular sciences · 2023Review
- Linc00662 mAmerican journal of cancer research · 2023Article
- Therapeutic Targeting the Allosteric Cysteinome of RAS and Kinase Families.Journal of molecular biology · 2022Review
- Shikonin inhibits the proliferation of cervical cancer cells via FAK/AKT/GSK3β signalling.Oncology letters · 2022Article
- PROTACs: great opportunities for academia and industry (an update from 2020 to 2021).Signal transduction and targeted therapy · 2022Review
- Identification of a Subset of Stage I Colorectal Cancer Patients With High Recurrence Risk.Journal of the National Cancer Institute · 2022Article
- Proteolysis-targeting chimeras (PROTACs) in cancer therapy.Molecular cancer · 2022Review
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- SIPA1 boosts migration and proliferation, and blocks apoptosis of glioma by activating the phosphorylation of the FAK signaling pathway.Journal of medical biochemistry · 2022Article
- Inhibitors, PROTACs and Molecular Glues as Diverse Therapeutic Modalities to Target Cyclin-Dependent Kinase.Cancers · 2021Review
- FAK inhibitors as promising anticancer targets: present and future directions.Future medicinal chemistry · 2021Review
- PROTACs to address the challenges facing small molecule inhibitors.European journal of medicinal chemistry · 2021Review
- An Update on Molecular Pathways Regulating Vasculogenic Mimicry in Human Osteosarcoma and Their Role in Canine Oncology.Frontiers in veterinary science · 2021Review
- PROTACs: An Emerging Therapeutic Modality in Precision Medicine.Cell chemical biology · 2020Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Focal adhesion kinase (FAK) is emerging as a promising cancer target because it is highly expressed at both the transcriptional and translational level in cancer and is involved in many aspects of tumor growth, invasion, and metastasis. Existing FAK-based therapeutics focus on inhibiting the kinase's catalytic function and not the large scaffold it creates that includes many oncogenic receptor tyrosine kinases and tumor suppressor proteins. Targeting the FAK scaffold is a feasible and promising approach for developing highly specific therapeutics that disrupt FAK signaling pathways in cancer.
Indexed as
Identifiers
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.