Related Experiment Video
Updated: Jun 8, 2026
Generation of CAR T Cells for Adoptive Therapy in the Context of Glioblastoma Standard of Care
Published on: February 16, 2015
Therapeutic exploitation of apoptosis and autophagy for glioblastoma
Donat Kögel1, Simone Fulda, Michel Mittelbronn
1Center for Neurology and Neurosurgery, Goethe University Hospital, Goethe University, Frankfurt, Germany. koegel@em.uni-frankfurt.de
Abstract:
Induction of caspase-dependent apoptosis (type I cell death) is a major mechanism by which most chemotherapeutic drugs and radiation kill tumor cells. However, conventional cancer therapies fail to mediate their effects in a target-specific fashion. The extremely unfavorable prognosis for patients suffering from glioblastomas (GBMs) is strongly correlated to the intrinsic apoptosis resistance of GBM cells which especially occurs in diffusely migrating tumor cells. The ultimate goal for molecular, apoptosis-based therapies is to target specific components of the two major apoptotic pathways, i.e. the extrinsic and the intrinsic pathway to trigger tumor-selective apoptosis, while at the same time limiting toxicity in normal tissues. Induction of autophagic cell death (type II cell death) by pro-autophagic drugs is an alternative and emerging concept to trigger glioma cell death and to exploit caspase-independent programmed cell death pathways for the development of novel glioma therapies. This review provides an up to date and comprehensive report on the relevant pre-clinical and clinical drugs interfering with the major apoptosis and autophagy pathways, their therapeutic potential in glioma and adresses potential future perspectives in this exciting field of research.
Insights
This review explores apoptosis and autophagy pathways for glioblastoma treatment. Targeting these programmed cell death pathways offers novel therapeutic strategies for glioma, aiming for tumor selectivity and reduced toxicity.
Area of Science:
- Oncology
- Molecular Biology
- Cell Death Pathways
Background:
- Conventional cancer therapies often lack tumor specificity, leading to significant toxicity.
- Glioblastomas (GBMs) exhibit intrinsic apoptosis resistance, particularly in migrating tumor cells, contributing to poor patient prognosis.
- Targeting specific apoptotic pathways (extrinsic and intrinsic) is crucial for developing tumor-selective therapies.
Purpose of the Study:
- To review pre-clinical and clinical drugs targeting apoptosis and autophagy pathways in glioma.
- To discuss the therapeutic potential of these agents in glioblastoma treatment.
- To explore future perspectives in molecularly targeted glioma therapies.
Main Methods:
- Comprehensive literature review of drugs affecting apoptosis and autophagy.
- Analysis of therapeutic strategies for glioblastoma.
- Examination of programmed cell death mechanisms (caspase-dependent and independent).
Main Results:
- Apoptosis induction is a primary mechanism for conventional cancer therapies.
- Autophagic cell death presents an alternative strategy for glioma cell death.
- Targeting specific pathways aims to enhance tumor selectivity and minimize normal tissue toxicity.
Conclusions:
- Molecularly targeted therapies focusing on apoptosis and autophagy pathways hold promise for glioblastoma treatment.
- Exploiting caspase-independent cell death pathways offers novel therapeutic avenues.
- Further research into these pathways could lead to improved glioma therapies with reduced side effects.
