ArticleCommunications engineering2024
Insights from a multiscale framework on metabolic rate variation driving glioblastoma multiforme growth and invasion.
Article in Communications engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 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.
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
2 citing papers in PubMed.
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- Tumoroid Model Reveals Synergistic Impairment of Metabolism by Iron Chelators and Temozolomide in Chemo-Resistant Patient-derived Glioblastoma Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-physiological levels of oxygen and nutrients within the tumors result in heterogeneous cell populations that exhibit distinct necrotic, hypoxic, and proliferative zones. Among these zonal cellular properties, metabolic rates strongly affect the overall growth and invasion of tumors. Here, we report on a hybrid discrete-continuum (HDC) mathematical framework that uses metabolic data from a biomimetic two-dimensional (2D) in-vitro cancer model to predict three-dimensional (3D) behaviour of in-vitro human glioblastoma (hGB). The mathematical model integrates modules of continuum, discrete, and neurons. Results indicated that the HDC model is capable of quantitatively predicting growth, invasion length, and the asymmetric finger-type invasion pattern in in-vitro hGB tumors. Additionally, the model could predict the reduction in invasion length of hGB tumoroids in response to temozolomide (TMZ). This model has the potential to incorporate additional modules, including immune cells and signaling pathways governing cancer/immune cell interactions, and can be used to investigate targeted therapies.
Identifiers
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Registered trials
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