Consistent with the present results, cellular senescence caused by gemcitabine was mediated by oxidative stress in pancreatic cancer cells.20 Furthermore, IR indirectly induced DNA damage mediated by increased ROS levels along with direct DNA damage, resulting in cellular senescence.21 Previous studies also demonstrated that gemcitabine prevented DNA repair by inhibiting DNA polymerase and Rad51-dependent DNA repair27,29; therefore, impaired DNA repair by gemcitabine may also contribute to increased DNA damage in senescent meningioma cells. This evidence concerns the gene RAD51 and familial pancreatic carcinoma.