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细胞周期靶向的药物筛选.ppt
Cell-cycle-targetingDrugs Sun Hong Pharm-Tox Team Introduction Many existing cancer chemotherapies interfere with DNA replication and formation of the mitotic spindle, that is, the processes central to the cell cycle. Alternative strategies aimed at targeting cell-cycle components that are specifically deregulated in tumour cells are now being explored. Several groups of protein kinases associated with aberrant tumour cell-cycle checkpoints are used as targets for the discovery of small-molecule inhibitor. The first of these compounds are now being evaluated in the clinic. Conventional cell-cycle-related strategies in oncology DNA-damaging agents Antimetabolites Topoisomerase inhibitors Agents that disrupt the microtubules of the mitotic spindle New cell-cycle-related strategies in oncology Normal cells rely on mitogenic stimulation to enter the cycle. Cancer cells enter and stay in cycle permanently, leading to the unchecked growth of tumours. Furthermore, DNA and spindle checkpoints are also frequently overridden in transformed cells. Reinstating cell-cycle control via pharmacological targeting of deregulated components of the checkpoint pathways should be a viable strategy in anticancer therapy. The mammalian cell cycle Cell-cycle-targeting Drugs Drugs targeting G1/S G2 checkpoint abrogators Mitosis and its drug targets Targeting G1/S The mainstay of cell-cycle-targeted therapeutic strategies,until recently, has been pharmacological reinstatement of G1/S checks in tumour cells. Early approaches were based on gene therapy with CDK-directed tumour-suppressor proteins. More recently, these indirect approaches have been supplanted by small-molecule agents, especially CDK inhibitors. G2 checkpoint abrogators The main purpose of the G2 checkpoint is to allow time for the cell to repair damaged DNA before mitotic entry. As a consequence of G1 checkpoint defects, tumour cells appear to depend on the G2 checkpoint more than no
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