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As most tumour cells have lost normal p53 function or inactivated its downstream pathways, the G1/S checkpoint is impaired and DNA damage repair is consequently dependent on ATR/Chk1-mediated intra-S and G2/M arrest (Soussi and Beroud, 2001

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A possible explanation for such observations may be that antioxidant systems are originally protective against tumorigenicity through a reduction in mutagenic ROS