{"title":"DNA损伤诱导的戊糖磷酸分流增强和化学抗性还原性应激的研究进展。","authors":"Chiara Milanese, Pier G Mastroberardino","doi":"10.1080/23723556.2020.1733383","DOIUrl":null,"url":null,"abstract":"<p><p>Metabolic rearrangements and genome instability are two hallmarks of cancer. Recent evidence from our laboratory demonstrates that persistent DNA lesions hampering transcription may cause glucose rerouting through the pentose phosphate shunt and reductive stress. Here, we highlight the relevance of these findings for cancer and chemoresistance development.</p>","PeriodicalId":520710,"journal":{"name":"Molecular & cellular oncology","volume":" ","pages":"1733383"},"PeriodicalIF":0.0000,"publicationDate":"2020-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23723556.2020.1733383","citationCount":"1","resultStr":"{\"title\":\"A perspective on DNA damage-induced potentiation of the pentose phosphate shunt and reductive stress in chemoresistance.\",\"authors\":\"Chiara Milanese, Pier G Mastroberardino\",\"doi\":\"10.1080/23723556.2020.1733383\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Metabolic rearrangements and genome instability are two hallmarks of cancer. Recent evidence from our laboratory demonstrates that persistent DNA lesions hampering transcription may cause glucose rerouting through the pentose phosphate shunt and reductive stress. Here, we highlight the relevance of these findings for cancer and chemoresistance development.</p>\",\"PeriodicalId\":520710,\"journal\":{\"name\":\"Molecular & cellular oncology\",\"volume\":\" \",\"pages\":\"1733383\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-03-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/23723556.2020.1733383\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular & cellular oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/23723556.2020.1733383\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular & cellular oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23723556.2020.1733383","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
A perspective on DNA damage-induced potentiation of the pentose phosphate shunt and reductive stress in chemoresistance.
Metabolic rearrangements and genome instability are two hallmarks of cancer. Recent evidence from our laboratory demonstrates that persistent DNA lesions hampering transcription may cause glucose rerouting through the pentose phosphate shunt and reductive stress. Here, we highlight the relevance of these findings for cancer and chemoresistance development.