Jul 2026· Cancer Research Communications· Vol 6, pp. 1898 - 1915· 0 citations· 64 references
Medicine
TL;DR
Mesenchymal tumors have aggressive migration but are immunologically “hot,” which suppresses net proliferation and may explain the lack of a strong survival difference between subtypes clinically, while also opening up new opportunities for subtype-specific therapies.
Abstract
Abstract Glioblastoma (GBM) remains a deadly cancer driven in part by invasion of tumor cells into the brain. Transcriptomic analyses have identified distinct molecular subtypes, but mechanistic differences that account for clinical differences are not clear. In this study, we show that, as predicted by the motor-clutch model of cell migration, mesenchymal glioma cells are more spread, generate larger traction forces, and migrate faster in brain tissue compared with proneural cells. Despite their rapid migration and comparable proliferation rates in vitro, mice with mesenchymal tumors survive longer than those with proneural tumors. This improved survival correlated with an immune response in mesenchymal tumors, including T cell–mediated. Consistently, inducing mesenchymal tumors in immunodeficient mice resulted in shorter survival, supporting a protective immune role in mesenchymal tumors. Thus, mesenchymal tumors have aggressive migration but are immunologically “hot,” which suppresses net proliferation. These two features counteract each other and may explain the lack of a strong survival difference between subtypes clinically, while also opening up new opportunities for subtype-specific therapies. Significance: This study highlights new mechanical and immunologic insights into GBM molecular subtypes using an integrated modeling–genome engineering strategy, which can potentially facilitate GBM subtype-specific therapeutic strategies.
The utility of ex vivo glioblastoma characterization is demonstrated, allowing decoding of tumor heterogeneity and clinical prognostication as well as providing a framework for deconvoluting the complex cancer phenotype.
Jay Hou, M. McMahon, Andrew Ni et al.· bioRxiv· 0 citations
Integrated analyses show that MBM exhibits dynamic bidirectional signaling across tumor cells, endothelium, and microglia, collectively driving invasion and proliferation.
Kevin Zhang, Mao Yang, Ming Yuang et al.· Neuro-Oncology Advances· 0 citations
The findings suggest that the progression to high-grade glioma relies less on cell-autonomous “stealth” mechanisms and more on the ability to tame and reprogram the immune microenvironment, thereby creating a tolerant, tumor-permissive niche.
Francesca Piaggio, Giorgia Guccione, Davide Ceresa et al.· Cell Communication and Signa...· 0 citations
An immunocompetent, autochthonous adult GBM mouse model driven by EGFRvIII expression with loss of PTEN and CDKN2A is developed and provides insight into how distinct immune populations respond to radiation therapy.
Emily A. Hatanaka, J. Breunig, S. Shiao et al.· Journal of Immunology· 0 citations
It is shown that surgical resection induces TREM2 associated immunosuppressive remodeling of the TME and CAR-T based strategies to reshape the perioperative GBM TME are tested.
Martin Pedard, Luis Castillo Cantero, Ali Ghasemi et al.· Nature Communications· 0 citations
Current strategies to reprogram innate immunity in GB are highlighted and key limitations that must be addressed are identified before innate immune-based approaches can be translated more effectively into clinical practice.
Lucas Everton Simões, Vitória Santório de São José, Vivaldo Moura et al.· Journal of Neuroimmunology· 0 citations
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