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Biomedicines
Special Issues
Glioma Therapy: Current Status and Future Prospects
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Glioma Therapy: Current Status and Future Prospects

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 64

Special Issue Editor

Prof. Dr. Bernd Kaina

E-Mail Website
Guest Editor
Department of Toxicology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany
Interests: DNA damage and repair; DNA damage response; mutagenesis and carcinogenesis; cell death mechanisms; glioma therapy; alkylating agents; cellular senescence; senotherapeutics

Special Issue Information

Dear Colleagues,

The most severe forms of brain cancer are glioma grades 3 and 4 (glioblastoma). The treatment of these tumors remains a challenge. Although many new findings have been made regarding the molecular biology of these tumors, not much has changed in standard therapy. Radiation and chemotherapy with temozolomide and/or CCNU are still considered the gold standard. Immunotherapy and kinase inhibitors have not yet become established in glioma therapy, although several clinical trials are running. This Special Issue will discuss new anticancer drugs and therapeutic strategies, including biomedical supportive therapies with natural compounds targeting autophagy, cell death, and senescence pathways.

Dr. Bernd Kaina
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

  • glioblastoma
  • temozolomide
  • nitrosoureas
  • immunotherapy
  • biologicals
  • tyrosine kinase inhibitors
  • senotherapeutics

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Published Papers (1 paper)

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Research

12 pages, 1031 KiB  
Article
IDH1 Mutation Impacts DNA Repair Through ALKBH2 Rendering Glioblastoma Cells Sensitive to Artesunate
by Olivier Switzeny, Stefan Pusch, Markus Christmann and Bernd Kaina
Biomedicines 2025, 13(6), 1479; https://doi.org/10.3390/biomedicines13061479 - 16 Jun 2025
Abstract
Background: Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are enzymes that catalyze the oxidative decarboxylation of isocitrate to alpha-ketoglutarate (α-KG), which is essential for many metabolic processes, including some steps in DNA repair. In tumors, notably in gliomas, IDH1 and IDH2 [...] Read more.
Background: Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are enzymes that catalyze the oxidative decarboxylation of isocitrate to alpha-ketoglutarate (α-KG), which is essential for many metabolic processes, including some steps in DNA repair. In tumors, notably in gliomas, IDH1 and IDH2 are frequently mutated. The mutation found in different cancers is functionally active, causing, instead of α-KG, the formation of 2-hydroxyglutarate (2-HG), which inhibits α-KG-dependent enzymes. Gliomas harboring mutated IDH1/2 show a better prognosis than IDH1 wild-type (wt) tumors of the same grade, which might result from the inhibition of DNA repair functions. A DNA repair enzyme dependent on α-KG is alkB homolog 2 (ALKBH2), which removes several lesions from DNA. These findings prompted us to investigate the response of glioma cells to artesunate (ART), a plant ingredient with genotoxic and anticancer activity currently used in several trials. Materials and Methods: We used isogenic glioblastoma cell lines that express IDH1 wild-type or, based on a TET-inducible system, the IDH1 mutant (mt) protein, and treated them with increasing doses of artesunate. We also treated glioblastoma cells with 2-HG, generated ALKBH2 knockout cells, and checked their sensitivity to the cytotoxic effects of artesunate. Results: We show that the cell-killing effect of ART is enhanced if the IDH1 mutant (R132H) is expressed in glioblastoma cells. Further, we show that 2-HG imitates the effect of IDH1mt as 2-HG ameliorates the cytotoxicity of ART. Finally, we demonstrate that the knockout of ALKBH2 causes the sensitization of glioblastoma cells to ART. Conclusions: The data indicate that ALKBH2 protects against the anticancer effect of ART, and the mutation of IDH1/2 commonly occurring in low-grade gliomas sensitizes to ART via an ALKBH2-dependent mechanism. The data support the use of ART in the therapy of IDH1/2-mutated cancers both in combination with chemotherapy and adjuvant treatment. Full article
(This article belongs to the Special Issue Glioma Therapy: Current Status and Future Prospects)
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