{"title":"结合DNA损伤剂和检查点1抑制剂。","authors":"Michelle Prudhomme","doi":"10.2174/1568011043352795","DOIUrl":null,"url":null,"abstract":"<p><p>During the cell cycle that leads to mitosis, checkpoints are activated in response to DNA damage. The checkpoints control the ability of cells to arrest the cell cycle allowing time to repair the DNA. In more than 50% of cancer cells, the G1 checkpoint is inactive due to mutations of p53. Therefore, the combination of a DNA damaging agent with a G2 checkpoint inhibitor should force selectively cancer cells into a premature and lethal mitosis. This approach which has recently drawn considerable interest is discussed in this paper.</p>","PeriodicalId":10914,"journal":{"name":"Current medicinal chemistry. Anti-cancer agents","volume":"4 5","pages":"435-8"},"PeriodicalIF":0.0000,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1568011043352795","citationCount":"18","resultStr":"{\"title\":\"Combining DNA damaging agents and checkpoint 1 inhibitors.\",\"authors\":\"Michelle Prudhomme\",\"doi\":\"10.2174/1568011043352795\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>During the cell cycle that leads to mitosis, checkpoints are activated in response to DNA damage. The checkpoints control the ability of cells to arrest the cell cycle allowing time to repair the DNA. In more than 50% of cancer cells, the G1 checkpoint is inactive due to mutations of p53. Therefore, the combination of a DNA damaging agent with a G2 checkpoint inhibitor should force selectively cancer cells into a premature and lethal mitosis. This approach which has recently drawn considerable interest is discussed in this paper.</p>\",\"PeriodicalId\":10914,\"journal\":{\"name\":\"Current medicinal chemistry. Anti-cancer agents\",\"volume\":\"4 5\",\"pages\":\"435-8\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2004-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.2174/1568011043352795\",\"citationCount\":\"18\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current medicinal chemistry. Anti-cancer agents\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/1568011043352795\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current medicinal chemistry. Anti-cancer agents","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1568011043352795","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Combining DNA damaging agents and checkpoint 1 inhibitors.
During the cell cycle that leads to mitosis, checkpoints are activated in response to DNA damage. The checkpoints control the ability of cells to arrest the cell cycle allowing time to repair the DNA. In more than 50% of cancer cells, the G1 checkpoint is inactive due to mutations of p53. Therefore, the combination of a DNA damaging agent with a G2 checkpoint inhibitor should force selectively cancer cells into a premature and lethal mitosis. This approach which has recently drawn considerable interest is discussed in this paper.
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