Glioblastoma

P1, N=5, Terminated, Nader Sanai | N=12 --> 5 | Trial completion date: May 2028 --> Oct 2025 | Recruiting --> Terminated; Study terminated due to unavailability of the investigational product required to continue the study.

P1, N=20, Active, not recruiting, City of Hope Medical Center | Trial completion date: Apr 2027 --> Sep 2026

P1, N=42, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Jul 2032 --> Nov 2028 | Trial primary completion date: Dec 2026 --> Nov 2028

P=N/A, N=15, Active, not recruiting, SonoClear AS | Recruiting --> Active, not recruiting | Trial primary completion date: Sep 2026 --> Jun 2026

P1, N=15, Active, not recruiting, University Hospital Muenster | Recruiting --> Active, not recruiting | Trial completion date: Apr 2026 --> Oct 2027 | Trial primary completion date: Apr 2026 --> Oct 2026

P1/2, N=28, Not yet recruiting, Erasmus Universitair Medisch Centrum Rotterdam (Erasmus MC)

P2/3, N=120, Active, not recruiting, Global Coalition For Adaptive Research Inc. | Recruiting --> Active, not recruiting

P2, N=25, Recruiting, Northwestern University | Trial completion date: Aug 2026 --> Aug 2031 | Trial primary completion date: May 2026 --> Jul 2031

P1, N=186, Not yet recruiting, Chipscreen Biosciences, Ltd.

We further emphasize emerging pharmacological strategies aimed at dismantling MISH by targeting these specific signaling pathways, thereby reprogramming TAAs from immunosuppressive barriers into potential allies for immunotherapy. Targeting MISH signaling networks represents a promising avenue to overcome resistance to current immunotherapies and improve outcomes for patients with brain tumors.

Using this lineage-resolved framework, we identify complementary drug targets in distinct progenitor compartments and demonstrate that hierarchy-informed combination therapies disrupt progenitor-progenitor interactions and reshape lineage output. These findings move beyond descriptive heterogeneity to define functional logic underlying GBM propagation and establish a generalizable framework for rational, cell type-specific combinatorial therapies.

These findings demonstrate that SPARCL1 expression in GBM is shaped by tumor architecture, molecular classification, and microenvironment interactions. Enrichment of SPARCl1 at invasive tumor margins is consistent with prior studies linking SPARCL1 to neuron-glioma synapse formation and angiogenesis.