Modularly tunable culture platforms mimicking the GSC niche maintained clinically relevant physiology of patient-derived GSCs ex vivo, including acquired resistance to EGFR inhibition and rapid infiltration. These biomaterial platforms provide a controlled experimental context in which to characterize how the GSC microenvironment facilitates GBM tumor aggression. Ultimately, we aim to identify specific GSC-ECM interactions whose targeted disruption represents a viable clinical strategy to prevent and/or delay both therapeutic resistance and vessel-mediated tumor infiltration.
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