ReviewCancers2025
The Role of Pyk2 Kinase in Glioblastoma Progression and Therapeutic Targeting.
Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Transcriptomic Reprogramming of the Human Placenta Following Maternal Opioid Exposure: Identification of Altered Metabolic and Translational Pathways.Current issues in molecular biology · 2026Article
- Computational identification of Cucurbitacin S and Kammogenin as bioactive focal adhesion kinase 2 inhibitors for targeted cancer therapy.Molecular diversity · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Glioblastoma (GBM) is a highly aggressive brain tumor with limited treatment options and poor prognosis. Proline-rich tyrosine kinase 2 (Pyk2) has been implicated in regulation of GBM invasion, proliferation, and recurrence. Its activation, driven by tumor-infiltrating microglia and macrophage-derived extracellular factors such as EGF, PDGFB, SDF-1α, IL-6, and IL-8, enhances tumor cell motility and survival. Experimental studies demonstrate that pharmacological inhibition or genetic knockdown of Pyk2 significantly reduces glioma cell migration and proliferation. Furthermore, recurrent GBM tumors exhibit elevated Pyk2 phosphorylation in mouse GBM models, correlating with increased tumor growth. Inhibition of Pyk2 and the structurally related focal adhesion kinase (FAK) signaling has shown promising results in preclinical studies, reducing tumor recurrence and improving survival outcomes. This review summarizes recent findings and underscores the pivotal role of Pyk2 in GBM pathophysiology, highlighting its potential as a therapeutic target.
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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.