The intracellular pathways activated by DNA damage lead to cell cycle arrest at different phases of the cell cycle thereby providing time to repair the lesions. In cancer cells, the G2 checkpoint arrest is especially important for surviving DNA damage since abrogation of G1 arrest, a common event in human malignancies, enhances the dependency of cells on an intact G2 checkpoint. However, despite the general idea that after DNA damage cells appear to enter a sustained arrest in the G2 phase of the cell cycle, it is still unclear whether this concept can be extended to all mammalian cell lines.
In the present study, a set of different mammalian cell lines were exposed to variable dosages of γ-radiation and the response to DNA damage was examined. The study shows that at equal dosages of γ-radiation the duration of G2 arrest varies widely. Moreover, the presence of a functional p53 not necessarily leads to a prolonged G2 arrest in the cell lines investigated. The reported results suggest that the G2 arrest response towards ionizing radiation is complex and that results generated from a single tissue culture cell line, may not be readily extrapolated to other cell lines or normal tissues.
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