ArticleCancer research2017
3D Mathematical Modeling of Glioblastoma Suggests That Transdifferentiated Vascular Endothelial Cells Mediate Resistance to Current Standard-of-Care Therapy.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 42 citations in OpenAlex.
- Prognostic model for pediatric brain tumors based on tumor microenvironment-specific gene signatures.Discover oncology · 2025Article
- Endothelial transdifferentiation of glioma stem cells: a literature review.Acta neuropathologica communications · 2025Review
- Agent-based modeling in cancer biomedicine: applications and tools for calibration and validation.Cancer biology & therapy · 2024Review
- Predicting the spatio-temporal response of recurrent glioblastoma treated with rhenium-186 labelled nanoliposomes.Brain multiphysics · 2023Article
- Data-driven spatio-temporal modelling of glioblastoma.Royal Society open science · 2023Review
- Glioblastoma-Specific Strategies of Vascularization: Implications in Anti-Angiogenic Therapy Resistance.Journal of personalized medicine · 2022Review
- Brain co-delivery of first-line chemotherapy drug and epigenetic bromodomain inhibitor for multidimensional enhanced synergistic glioblastoma therapy.Exploration (Beijing, China) · 2022Article
- Agent-based computational modeling of glioblastoma predicts that stromal density is central to oncolytic virus efficacy.iScience · 2022Article
- Impact of Regorafenib on Endothelial Transdifferentiation of Glioblastoma Stem-like Cells.Cancers · 2022Article
- Modelling glioma progression, mass effect and intracranial pressure in patient anatomy.Journal of the Royal Society, Interface · 2022Article
- Bioengineered Models to Study Microenvironmental Regulation of Glioblastoma Metabolism.Journal of neuropathology and experimental neurology · 2021Review
- Bioprinting Scaffolds for Vascular Tissues and Tissue Vascularization.Bioengineering (Basel, Switzerland) · 2021Review
- Elesclomol-induced increase of mitochondrial reactive oxygen species impairs glioblastoma stem-like cell survival and tumor growth.Journal of experimental & clinical cancer research : CR · 2021Article
- Article
- Ionizing radiation induces endothelial transdifferentiation of glioblastoma stem-like cells through the Tie2 signaling pathway.Cell death & disease · 2019Article
- Personalized Radiotherapy Design for Glioblastoma: Integrating Mathematical Tumor Models, Multimodal Scans, and Bayesian Inference.IEEE transactions on medical imaging · 2019Article
- Glioblastoma Stem Cells and Comparison of Isolation Methods.Journal of clinical medicine research · 2019Article
- Glioblastoma Stem-Frontiers in oncology · 2019Review
- BMP9 counteracts the tumorigenic and pro-angiogenic potential of glioblastoma.Cell death and differentiation · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM), the most aggressive brain tumor in human patients, is decidedly heterogeneous and highly vascularized. Glioma stem/initiating cells (GSC) are found to play a crucial role by increasing cancer aggressiveness and promoting resistance to therapy. Recently, cross-talk between GSC and vascular endothelial cells has been shown to significantly promote GSC self-renewal and tumor progression. Furthermore, GSC also transdifferentiate into bona fide vascular endothelial cells (GEC), which inherit mutations present in GSC and are resistant to traditional antiangiogenic therapies. Here we use three-dimensional mathematical modeling to investigate GBM progression and response to therapy. The model predicted that GSCs drive invasive fingering and that GEC spontaneously form a network within the hypoxic core, consistent with published experimental findings. Standard-of-care treatments using DNA-targeted therapy (radiation/chemo) together with antiangiogenic therapies reduced GBM tumor size but increased invasiveness. Anti-GEC treatments blocked the GEC support of GSCs and reduced tumor size but led to increased invasiveness. Anti-GSC therapies that promote differentiation or disturb the stem cell niche effectively reduced tumor invasiveness and size, but were ultimately limited in reducing tumor size because GECs maintain GSCs. Our study suggests that a combinatorial regimen targeting the vasculature, GSCs, and GECs, using drugs already approved by the FDA, can reduce both tumor size and invasiveness and could lead to tumor eradication.
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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.