ArticleInternational journal of molecular sciences2023
Pyk2/FAK Signaling Is Upregulated in Recurrent Glioblastoma Tumors in a C57BL/6/GL261 Glioma Implantation Model.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Phase I Evaluation of Patients with Newly Diagnosed Glioblastoma Treated with Radiation, Nivolumab, and IDO1 Enzyme Inhibitor BMS-986205.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models.iScience · 2026Article
- The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study.Translational oncology · 2026Article
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- Window of opportunity study measuring defactinib and avutometinib delivery in glioblastomas.Cancer chemotherapy and pharmacology · 2026Article
- Review
- Drug Combinations Targeting FAK and MEK Overcomes Tumor Heterogeneity in Glioblastoma.Pharmaceutics · 2025Article
- Context-specific targeting of focal adhesion kinase in brain tumors: lessons from glioblastoma and neurofibromatosis type 2-mutant meningioma.Frontiers in oncology · 2025Review
- The Role and Applied Value of Mitochondria in Glioma-Related Research.CNS neuroscience & therapeutics · 2024Review
- Tailoring glioblastoma treatment based on longitudinal analysis of post-surgical tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2024Article
- The Potential Role of the Extracellular Matrix Glycoprotein Reelin in Glioblastoma Biology.Pharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The majority of glioblastomas (GBMs) recur shortly after tumor resection and recurrent tumors differ significantly from newly diagnosed GBMs, phenotypically and genetically. In this study, using a Gl261-C57Bl/6 mouse glioma implantation model, we identified significant upregulation of proline-rich tyrosine kinase Pyk2 and focal adhesion kinase (FAK) phosphorylation levels-pPyk2 (579/580) and pFAK (925)-without significant modifications in total Pyk2 and FAK protein expression in tumors regrown after surgical resection, compared with primary implanted tumors. Previously, we demonstrated that Pyk2 and FAK are involved in the regulation of tumor cell invasion and proliferation and are associated with reduced overall survival. We hypothesized that the use of inhibitors of Pyk2/FAK in the postsurgical period may reduce the growth of recurrent tumors. Using Western blot analysis and confocal immunofluorescence approaches, we demonstrated upregulation of Cyclin D1 and the Ki67 proliferation index in tumors regrown after resection, compared with primary implanted tumors. Treatment with Pyk2/FAK inhibitor PF-562271, administered through oral gavage at 50 mg/kg daily for two weeks beginning 2 days before tumor resection, reversed Pyk2/FAK signaling upregulation in recurrent tumors, reduced tumor volume, and increased animal survival. In conclusion, the use of Pyk2/FAK inhibitors can contribute to a delay in GBM tumor regrowth after surgical resection.
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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 Socratic graph.