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  [Masanobu Takahashi,Minoru Koi et al. JBC 2011 April;286:12157-12165]

  in vivo suppression of PAR formation by the PARP inhibitor AZD2281 upon induction of DNA damage Primary human lung fibroblast cells (MRC-5) were pre-treated with the indicated concentration of the PARP inhibitor AZD2281 for two hours. Oxidative DNA damage was induced by 500 µM H2O2 for 10 min and cellular PARP activity was measured by immuno-staining of poly(ADP)-ribose (PAR) (right panels). The in vivo effect of PARP inhibition was compared to cells without DNA damage induction and inhibitor (control) and H2O2-treated cells without inhibitor. Average nuclear PAR staining intensities of more than 50 cells were statistically analysed by Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests (left panel). Asterisks indicate highly significant (p<1%) differences to H2O2-treated cells without PARP inhibitor. Thick horizontal bars mark medians and error bars the interquartile range.
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  [Katharina Schlacher,Nicole Christ et al Cell 2011.May;145:529-42]

  Effect of AZD 2281 on the viability of endometrial cancer cell line Hec50 and Ishikawa and ovarian cancer cell line SKOV3,Caov3 and PA-1 was detected by WST-1 method after 3 days treatment.
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  [Junko Murai, Kailin Yang et al Mol Cell Biol 2011.June;31:2462-9]

  MSH3-deficient cells are sensitive to olaparib, aPARPinhibitor, and the combination with oxaliplatin. A, clonogenic survival of HCT11635, G5 without doxycycline (DOX), and G5 cells with doxycycline, which were treated with 2M of oxaliplatin, 2M of olaparib, and the combination of these two drugs. B, clonogenic survival of HT29 cells, which were treated with 1 M oxaliplatin, 2 M olaparib, and the combination of these two drugs.