Cell-based therapies for malignant glioma.
- 1Department of Stem Cell Biology and Regenerative Medicine, City of Hope Comprehensive Cancer Center and Beckman Research Institute, Duarte, CA 91010, United States.
- 2Department of Medical Oncology, University Hospitals and Case Western Reserve University, Cleveland, OH 44106, United States.
Abstract
Despite innovative progress, cellular therapies have not produced durable, population-level survival gains in glioblastoma. Across 3 major modalities, engineered effectors such as chimeric antigen receptor T cell (CAR-T) and natural killer (NK) cells, immune-education platforms such as dendritic and whole-cell vaccines, and carrier cells delivering oncolytic or drug payloads, trials have shown measurable bioactivity, but durability has varied. This likely reflects systemic barriers, including therapy-induced lymphopenia, myeloid dominance, and T-cell sequestration, as well as local barriers such as antigen heterogeneity and immune suppression. To understand why some studies nevertheless showed more favorable efficacy signals, we reviewed clinical outcomes across these modalities and identified 4 recurring design features that appeared repeatedly among studies reporting more favorable survival signals: treatment in the minimal residual disease setting, a T-helper type 1 supportive context, broadened antigenic coverage, and effective immune hand-off from the initiating therapy to endogenous or adoptively transferred effectors. Across heterogeneous early-phase studies, greater feature alignment sometimes co-occurred with more favorable signals, although this retrospective pattern is descriptive and does not establish association or causality. These observations may help guide future biomarker-informed strategies and provide a practical framework for organizing multimodal trials aimed at converting transient bioactivity into more durable, polyclonal control.
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BibTeX
@article{mooney2026cellbased,
title = {{Cell-based therapies for malignant glioma.}},
author = {Rachael Mooney and Eslam E Abd El-Fattah and Gary Ngai and Jacqueline Lara and Mohamed Hammad and Karen S Aboody},
journal = {Stem cells translational medicine},
year = {2026},
month = oct,
doi = {10.1093/stcltm/szag084},
url = {https://europepmc.org/article/MED/42907136},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Cell-based therapies for malignant glioma.
AU - Rachael Mooney
AU - Eslam E Abd El-Fattah
AU - Gary Ngai
AU - Jacqueline Lara
AU - Mohamed Hammad
AU - Karen S Aboody
PY - 2026
DA - 2026/10/01
JO - Stem cells translational medicine
DO - 10.1093/stcltm/szag084
UR - https://europepmc.org/article/MED/42907136
AB - Despite innovative progress, cellular therapies have not produced durable, population-level survival gains in glioblastoma. Across 3 major modalities, engineered effectors such as chimeric antigen receptor T cell (CAR-T) and natural killer (NK) cells, immune-education platforms such as dendritic and whole-cell vaccines, and carrier cells delivering oncolytic or drug payloads, trials have shown measurable bioactivity, but durability has varied. This likely reflects systemic barriers, including therapy-induced lymphopenia, myeloid dominance, and T-cell sequestration, as well as local barriers such as antigen heterogeneity and immune suppression. To understand why some studies nevertheless showed more favorable efficacy signals, we reviewed clinical outcomes across these modalities and identified 4 recurring design features that appeared repeatedly among studies reporting more favorable survival signals: treatment in the minimal residual disease setting, a T-helper type 1 supportive context, broadened antigenic coverage, and effective immune hand-off from the initiating therapy to endogenous or adoptively transferred effectors. Across heterogeneous early-phase studies, greater feature alignment sometimes co-occurred with more favorable signals, although this retrospective pattern is descriptive and does not establish association or causality. These observations may help guide future biomarker-informed strategies and provide a practical framework for organizing multimodal trials aimed at converting transient bioactivity into more durable, polyclonal control.
SN - 2157-6564
SN - 2157-6580
ER -