Targeting DNA double-strand break repair for glioblastoma chemotherapy

Teodora Nikolova, Oliver H. Kramer

 

Institute of Toxicology, University Medical Center, Mainz, Germany

 

Corresponding author: Institute of Toxicology, University Medical Center Mainz, Obere Zahlbacher Str. 67, D-55131 Mainz, Germany, okraemer@uni-mainz.de

 

Citation: Oliver H. Kramer (2019) Targeting DNA double-strand break repair for glioblastoma chemotherapy. Sci World J Cancer Sci Ther, 1(1);1-4

 

Copyright: ©2019, Oliver H. Kramer, This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

 

ABSTRACT

 

Glioblastoma Multiforme(GBM) is the most prevalent primary malignant brain tumor in adults. Despite improvements in surgery, irradiation, and chemotherapeutic treatments, GBM remains a clinically unresolved problem. We sum up how GBM is currently treated, with a focus on temozolomide (TMZ) and chloronitrosoureas. We condense how such agents evoke lethal DNA damage in transformed cells and how these counteract such mechanisms. A better knowledge of such pathways may pave the way for improved therapies. Therefore, we recapitulate how inhibitors of the DNA repair factors PARP and RAD51 as well as epigenetic modulators of the histone deacetylase (HDAC) family might be useful in combination with established methylating and alkylating agents against GBM.

 

KEYWORDS: Alkylating agents, DNA damage, HDAC, Glioblastoma, PARP, RAD51

 

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