ArticleCancer research2010
Conditional deletion of the focal adhesion kinase FAK alters remodeling of the blood-brain barrier in glioma.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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.
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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.
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Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- MRAS: Master Regulator Analysis of Alternative Splicing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Tight junction proteins in glial tumors development and progression.Frontiers in cellular neuroscience · 2025Review
- COL8A1 overexpression promotes glioma cell growth by activating focal adhesion kinase signaling cascade.NPJ precision oncology · 2024Article
- Mouse Models to Evaluate the Functional Role of the Tumor Microenvironment in Cancer Progression and Therapy Responses.Cold Spring Harbor perspectives in medicine · 2024Review
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Conditional expression of endorepellin in the tumor vasculature attenuates breast cancer growth, angiogenesis and hyaluronan deposition.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Article
- Functional and clinical characteristics of focal adhesion kinases in cancer progression.Frontiers in cell and developmental biology · 2022Review
- Blood-brain barrier-restricted translocation ofeLife · 2021Article
- Phosphorylation of pericyte FAK-Y861 affects tumour cell apoptosis and tumour blood vessel regression.Angiogenesis · 2021Article
- Review
- Association of Low Tumor Endothelial Cell pY397-Focal Adhesion Kinase Expression With Survival in Patients With Neoadjuvant-Treated Locally Advanced Breast Cancer.JAMA network open · 2020Article
- Pericyte FAK negatively regulates Gas6/Axl signalling to suppress tumour angiogenesis and tumour growth.Nature communications · 2020Article
- Targeting focal adhesion kinase in cancer cells and the tumor microenvironment.Experimental & molecular medicine · 2020Review
- Neutrophil-Derived Reactive Oxygen Orchestrates Epithelial Cell Signaling Events during Intestinal Repair.The American journal of pathology · 2019Article
- Angiopoietin-2 exacerbates cardiac hypoxia and inflammation after myocardial infarction.The Journal of clinical investigation · 2018Article
- Prognostic significance of c-Met, β-catenin and FAK in patients with hepatocellular carcinoma following surgery.Oncology letters · 2018Article
- Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability.Circulation research · 2017Review
- A dynamic in vivo-like organotypic blood-brain barrier model to probe metastatic brain tumors.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Gliomas generally infiltrate the surrounding normal brain parenchyma, a process associated with increased vascular permeability (VP) and dysregulation of the blood-brain barrier (BBB). However, the molecular mechanisms underlying glioma-induced VP in the brain remain poorly understood. Using a conditional, endothelium-specific deletion of the focal adhesion kinase (FAK) in the mouse (FAK CKO), we show that FAK is critical for destabilization of the tumor endothelium in tumor-bearing mice, with mutant mice exhibiting a relatively normalized vasculature compared with wild-type mice (FAK WT). Tumor vessels in the FAK CKO mice displayed reduced VP compared with FAK WT mice, resulting in reduced tumor growth. Additionally, FAK CKO mice displayed partial restoration of cell-cell junction proteins in the tumor vessels and astrocyte-endothelium interactions in tumors, revealing an additional role of astrocytes in mediating tumor-induced VP. Together, these results provide genetic evidence that FAK is a mediator of tumor-induced VP in the brain. Our findings may help understand how therapeutics might be used to regulate specific cell-type interactions to restore BBB structure/function in cancer and perhaps other pathologic conditions.
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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.