Similarly, in synchronously growing cell populations originating from collected mitotic cells, growth delay is also strongly dependent on the cell-cycle phase at which cells were irradiated. Various drugs have also been used to generate synchronous cell populations. However, imperfections in synchronization, redistribution anti relief synchronization, and the side effects of drugs pose technical challenges to the interpretation of these experiments; for instance, hydroxyurea induces massive Genipin amounts of DNA double-strand breaks. Furthermore, when cells are simultaneously irradiated under asynchronous conditions, independent analysis of each separate population makes it difficult to compare and reconstruct cell-cycle kinetics. Therefore, cell-cycle markers that can be visualized in living cells, in combination with time-lapse imaging, would allow us to overcome such issues and obtain more precise information. In addition to cell-cycle check points, endoreduplication occurs inp53-deficientcancer cells after exposure to high doses of ionizing radiation or etoposide: specifically, cells skipmitos is after irradiation, resulting in multiple rounds of DNA replication and chromoso mesegregation without cytokinesis, giving rise to endo polyploid giant cells.p21 is transcriptionally activated byp53 after irradiation, and is thought to play apivotal role in inhibiting endoreduplication. However, cells with functional p53 are also likely to exhibit endoreduplication following exposure to DNA-damaging agents ,Primidone including irradiation an detoposide, depending on the extent of the damage. Therefore, irrespective of p53 status, we must carefully observe whether endoreduplication occurs in order to precisely interpret radiation-induced cell-cycle kinetics. Levels of the Cdt1 protein, a DNA replication licensing factor, are regulated along with the cell cycle by theE3 ligase SCFSkp2,enabling specific expression of Cdt1 in G1phase. On the other hand, Geminin is an inhibitor of Cdt1 whose levels are regulated by another E3 ligase,APCCdh1,enabling expression of this protein in the S/G2/M phases.