作者: Alessandra Blasina , Brendan D. Price , Gaetan A. Turenne , Clare H. McGowan
DOI: 10.1016/S0960-9822(99)80486-2
关键词:
摘要: The basis of many anti-cancer therapies is the use genotoxic agents that damage DNA and thus kill dividing cells. Agents cause cells to override DNA-damage checkpoint are predicted sensitize killing by agents. They have therefore been sought as adjuncts in radiation therapy chemotherapy. One such compound, caffeine, uncouples cell-cycle progression from replication repair [1] [2]. Caffeine servers a model compound establishing principle checkpoints can be used effects drugs [3]. But despite more than 20 years use, molecular mechanisms which caffeine affects cell cycle responses not identified. We investigated on G2/M human report radiation-induced activation kinase Cds1 [4] (also known Chk2 [5]) inhibited vivo ATM activity directly vitro. Inhibition provides explanation attenuation for increased radiosensitivity caffeine-treated [6] [7] [8].