02806nas a2200421   4500000000100000000000100001008004100002260000900043653001700052653001700069653002500086653003100111653002800142100001500170700002400185700001600209700001900225700001500244700001700259700001400276700002000290700001900310700001700329700001600346700001900362700001800381700002000399700002600419700002200445700001500467700001700482245014900499856006700648300001100715490000700726520163700733022001402370       2026                            d  c202610aglioblastoma10ainvasiveness10aorganoid fabrication10atumor extracellular matrix10atumor-host interactions1 aChao Liang1 aHenry Robert Howard1 aShihui Chen1 aWon-Young Choi1 aSummer Cao1 aArthur Chien1 aKevin Zou1 aMichael Kassiou1 aFabien Delerue1 aHo Sang Jung1 aYeonju Park1 aYoung Mee Jung1 aYong-Dae Kwon1 aKarrie M. Kiang1 aGilberto Ka-Kit Leung1 aRyohichi Sugimura1 aAnn-Na Cho1 aSang Jin Lee00aFlash Assembloids: A Rapid Biofabrication of a Platform for Modeling Early Glioblastoma Invasion at the Glioblastoma–Brain Organoid Interfaces  uhttps://onlinelibrary.wiley.com/doi/abs/10.1002/adhm.202504842  ae048420 v153 aGlioblastoma (GBM) remains one of the most aggressive brain malignancies, characterized by rapid infiltration, therapeutic resistance, and dismal prognosis. Modeling GBM invasion in physiologically relevant systems has been hindered by the lack of reproducible platforms. Here, we present a bioengineered assembloid (ASM) system that integrates GBM cells encapsulated in self-degradable 5% oxidized alginate microgel (5OA) with dorsal forebrain organoids (DOs) to recapitulate early tumor-host interactions during glioblastoma invasion toward the brain. Live-cell imaging revealed GBM self-aggregation, leading to increased recruitment and invasion at the DO boundary, accompanied by strong cell-cell adhesion, nuclear compaction, and the infiltration fronts enriched in SOX2+/Vimentin+ tumor populations. Transcriptomic profiling demonstrated upregulation of adhesion, integrin clustering, and mechanosensing-associated genes, alongside downregulation of neuronal differentiation pathways, indicating a dual invasion and host suppression strategy. Comparative analyses of GBM-only constructs and DO-GBM ASMs revealed elevated expression of laminin subunits and enrichment of invasion-associated pathways, including PI3K-AKT-mTOR and TGF-β signaling, reflecting a shift toward an invasive state at the transcriptomic level. In vivo implantation of ASMs confirmed aggressive GBM infiltration and niche remodeling, highlighting the translational relevance. These findings suggest that it recapitulates the structural, molecular, and functional hallmarks of GBM invasion and tumor-driven remodeling of the host brain microenvironment.  a2192-2659