Honglin Jiang, Ryan K Muir, R. Gonciarz, A. Olshen, I. Yeh, B. Hann, Ning Zhao, Yung-hua Wang, S. Behr, J. Korkola, M. Evans, E. Collisson, A. Renslo
{"title":"亚铁活化药物偶联在kras驱动的肿瘤中实现有效的MAPK阻断","authors":"Honglin Jiang, Ryan K Muir, R. Gonciarz, A. Olshen, I. Yeh, B. Hann, Ning Zhao, Yung-hua Wang, S. Behr, J. Korkola, M. Evans, E. Collisson, A. Renslo","doi":"10.1084/jem.20210739","DOIUrl":null,"url":null,"abstract":"Jiang et al. report that oncogenic KRAS signaling induces ferrous iron (Fe2+) accumulation throughout mutant KRAS-mediated transformation. Converting an FDA-approved MEK inhibitor into a ferrous iron–activatable drug conjugate (FeADC) achieves potent MAPK blockade in tumor cells with superior systemic tolerability.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"12","resultStr":"{\"title\":\"Ferrous iron–activatable drug conjugate achieves potent MAPK blockade in KRAS-driven tumors\",\"authors\":\"Honglin Jiang, Ryan K Muir, R. Gonciarz, A. Olshen, I. Yeh, B. Hann, Ning Zhao, Yung-hua Wang, S. Behr, J. Korkola, M. Evans, E. Collisson, A. Renslo\",\"doi\":\"10.1084/jem.20210739\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Jiang et al. report that oncogenic KRAS signaling induces ferrous iron (Fe2+) accumulation throughout mutant KRAS-mediated transformation. Converting an FDA-approved MEK inhibitor into a ferrous iron–activatable drug conjugate (FeADC) achieves potent MAPK blockade in tumor cells with superior systemic tolerability.\",\"PeriodicalId\":23015,\"journal\":{\"name\":\"The Tokushima journal of experimental medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-03-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"12\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Tokushima journal of experimental medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1084/jem.20210739\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Tokushima journal of experimental medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1084/jem.20210739","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ferrous iron–activatable drug conjugate achieves potent MAPK blockade in KRAS-driven tumors
Jiang et al. report that oncogenic KRAS signaling induces ferrous iron (Fe2+) accumulation throughout mutant KRAS-mediated transformation. Converting an FDA-approved MEK inhibitor into a ferrous iron–activatable drug conjugate (FeADC) achieves potent MAPK blockade in tumor cells with superior systemic tolerability.