ArticleActa neuropathologica communications2024
Laminin-associated integrins mediate Diffuse Intrinsic Pontine Glioma infiltration and therapy response within a neural assembloid model.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Biofabrication for spatial control of multiscale biological crosstalk in tissue models.npj biomedical innovations · 2026Review
- Immunotherapy for Diffuse Midline Glioma: From Preclinical Modeling to Clinical Translation.Cancers · 2026Review
- Microglia in diffuse midline glioma contribute to extracellular matrix remodelling and cancer cell invasion.Cell death & disease · 2026Article
- Consequences of irradiation on blood-brain tumor barrier model of Diffuse Midline Glioma: characterization of physical and metabolic properties.Fluids and barriers of the CNS · 2026Article
- Recreating the human brain: Are assembloids merely descriptive models?Frontiers in cellular neuroscience · 2026Review
- Novel Diffuse Midline Glioma-on-Chip Recapitulating Tumor Biophysical Microenvironment to Assess the Heterogeneity of Response to Therapies.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Extracellular matrix dynamics in tumor immunoregulation: from tumor microenvironment to immunotherapy.Journal of hematology & oncology · 2025Review
- Glioblastoma-derived migrasomes promote migration and invasion by releasing PAK4 and LAMA4.Communications biology · 2025Article
- The therapeutic potential of repurposed mebendazole, alone and in synergistic combination with ONC201, in the treatment of diffuse midline glioma.American journal of cancer research · 2025Article
- Glioma actively orchestrate a self-advantageous extracellular matrix to promote recurrence and progression.BMC cancer · 2024Review
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11 authors.
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Abstract
Diffuse Intrinsic Pontine Glioma (DIPG) is a highly aggressive and fatal pediatric brain cancer. One pre-requisite for tumor cells to infiltrate is adhesion to extracellular matrix (ECM) components. However, it remains largely unknown which ECM proteins are critical in enabling DIPG adhesion and migration and which integrin receptors mediate these processes. Here, we identify laminin as a key ECM protein that supports robust DIPG cell adhesion and migration. To study DIPG infiltration, we developed a DIPG-neural assembloid model, which is composed of a DIPG spheroid fused to a human induced pluripotent stem cell-derived neural organoid. Using this assembloid model, we demonstrate that knockdown of laminin-associated integrins significantly impedes DIPG infiltration. Moreover, laminin-associated integrin knockdown improves DIPG response to radiation and HDAC inhibitor treatment within the DIPG-neural assembloids. These findings reveal the critical role of laminin-associated integrins in mediating DIPG progression and drug response. The results also provide evidence that disrupting integrin receptors may offer a novel therapeutic strategy to enhance DIPG treatment outcomes. Finally, these results establish DIPG-neural assembloid models as a powerful tool to study DIPG disease progression and enable drug discovery.
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