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  • A role for homologous recombination and abnormal cell-cycle progression in radioresistance of glioma-initiating cells

    Author(s)
    Lim, Yi Chieh
    Roberts, Tara
    Day, Bryan
    Harding, Angus
    Kozlov, Sergei
    Kijas, Amanda
    Ensbey, Kathleen
    Walker, David
    Lavin, Martin
    Griffith University Author(s)
    Walker, David G.
    Year published
    2012
    Metadata
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    Abstract
    Glioblastoma multiforme (GBM) is the most common form of brain tumor with a poor prognosis and resistance to radiotherapy. Recent evidence suggests that glioma-initiating cells play a central role in radioresistance through DNA damage checkpoint activation and enhanced DNA repair. To investigate this in more detail, we compared the DNA damage response in nontumor forming neural progenitor cells (NPC) and glioma-initiating cells isolated from GBM patient specimens. As observed for GBM tumors, initial characterization showed that glioma-initiating cells have long-term self-renewal capacity. They express markers identical to ...
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    Glioblastoma multiforme (GBM) is the most common form of brain tumor with a poor prognosis and resistance to radiotherapy. Recent evidence suggests that glioma-initiating cells play a central role in radioresistance through DNA damage checkpoint activation and enhanced DNA repair. To investigate this in more detail, we compared the DNA damage response in nontumor forming neural progenitor cells (NPC) and glioma-initiating cells isolated from GBM patient specimens. As observed for GBM tumors, initial characterization showed that glioma-initiating cells have long-term self-renewal capacity. They express markers identical to NPCs and have the ability to form tumors in an animal model. In addition, these cells are radioresistant to varying degrees, which could not be explained by enhanced nonhomologous end joining (NHEJ). Indeed, NHEJ in glioma-initiating cells was equivalent, or in some cases reduced, as compared with NPCs. However, there was evidence for more efficient homologous recombination repair in glioma-initiating cells. We did not observe a prolonged cell cycle nor enhanced basal activation of checkpoint proteins as reported previously. Rather, cell-cycle defects in the G1-S and S-phase checkpoints were observed by determining entry into S-phase and radioresistant DNA synthesis following irradiation. These data suggest that homologous recombination and cell-cycle checkpoint abnormalities may contribute to the radioresistance of glioma-initiating cells and that both processes may be suitable targets for therapy.
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    Journal Title
    Molecular Cancer Therapeutics
    Volume
    11
    Issue
    9
    DOI
    https://doi.org/10.1158/1535-7163.MCT-11-1044
    Subject
    Oncology and carcinogenesis
    Pharmacology and pharmaceutical sciences
    Publication URI
    http://hdl.handle.net/10072/53208
    Collection
    • Journal articles

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