ArticleJournal of biosciences2026
Computational insights into cancer stem cell dynamics and the urokinase plasminogen activation pathway.
Article in Journal of biosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
This study introduces a novel computational model that integrates cancer stem cells (CSCs) and the plasminogen activation system, filling a crucial gap in cancer research. While theoretical models have separately explored CSCs and the plasminogen activation system, no prior computational framework has combined these elements. Our model focuses on the invasion dynamics of CSCs, emphasizing the critical interactions between urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1). We employed reaction-diffusion equations and analyzed the determinant and eigenvalue spectra of the Jacobian matrix of the system to identify instability regions within tumors. The findings revealed that the production and binding of uPA and PAI-1 significantly enhance the invasiveness and motility of CSCs, resulting in more complex and aggressive tumor structures. Our study advances the theoretical understanding of cancer dynamics by integrating these two critical biological processes into a single computational framework. This work builds upon and extends previous models by offering a more comprehensive analysis of tumor growth, with significant implications for optimizing cancer treatment strategies. The insights of the model into the interplay between CSCs and the plasminogen activation system offer a valuable tool for both research and potential clinical applications, paving the way for more targeted and effective therapeutic approaches.
Indexed as
Identifiers
42100976What 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.