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Updated: Mar 8, 2026

Generation of CAR T Cells for Adoptive Therapy in the Context of Glioblastoma Standard of Care
Published on: February 16, 2015
Advances in epigenetic glioblastoma therapy
Dong Hoon Lee1,2, Hyun-Wook Ryu1, Hye-Rim Won1
1College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Incheon, Republic of Korea.
Abstract:
Glioblastoma multiforme (GBM) is the most lethal primary brain tumor in adults despite contemporary gold-standard first-line treatment strategies. This type of tumor recurs in virtually all patients and no commonly accepted standard treatment exists for the recurrent disease. Therefore, advances in all scientific and clinical aspects of GBM are urgently needed. Epigenetic mechanisms are one of the major factors contributing to the pathogenesis of cancers, including glioblastoma. Epigenetic modulators that regulate gene expression by altering the epigenome and non-histone proteins are being exploited as therapeutic drug targets. Over the last decade, numerous preclinical and clinical studies on histone deacetylase (HDAC) inhibitors have shown promising results in various cancers. This article provides an overview of the anticancer mechanisms of HDAC inhibitors and the role of HDAC isoforms in GBM. We also summarize current knowledge on HDAC inhibitors on the basis of preclinical studies and emerging clinical data.
Insights
Histone deacetylase (HDAC) inhibitors show promise for treating glioblastoma multiforme (GBM), a deadly brain cancer. Research explores their anticancer mechanisms and role in recurrent GBM therapy.
Area of Science:
- Neuro-oncology
- Cancer epigenetics
- Pharmacology
Background:
- Glioblastoma multiforme (GBM) is an aggressive primary brain tumor with poor prognosis.
- Recurrent GBM lacks standard effective treatments, necessitating novel therapeutic strategies.
- Epigenetic dysregulation is a key driver in GBM pathogenesis.
Purpose of the Study:
- To provide an overview of the anticancer mechanisms of histone deacetylase (HDAC) inhibitors.
- To elucidate the role of specific HDAC isoforms in GBM.
- To summarize preclinical and clinical data on HDAC inhibitors for GBM treatment.
Main Methods:
- Review of preclinical studies investigating HDAC inhibitors in GBM models.
- Analysis of clinical trial data for HDAC inhibitors in cancer, with a focus on GBM.
- Examination of the molecular mechanisms of HDAC inhibition in cancer epigenetics.
Main Results:
- HDAC inhibitors demonstrate broad anticancer activities by modulating gene expression and protein function.
- Specific HDAC isoforms are implicated in GBM development and progression.
- Preclinical data suggest therapeutic potential, with ongoing clinical investigations.
Conclusions:
- HDAC inhibitors represent a promising therapeutic avenue for glioblastoma, particularly for recurrent disease.
- Targeting epigenetic mechanisms offers a novel approach to combat GBM.
- Further research and clinical trials are warranted to optimize HDAC inhibitor therapy for GBM patients.
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