亚铁活化药物偶联在kras驱动的肿瘤中实现有效的MAPK阻断

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}
引用次数: 12

摘要

Jiang等人报道,在KRAS介导的突变体转化过程中,致癌KRAS信号传导诱导亚铁(Fe2+)积累。将fda批准的MEK抑制剂转化为亚铁活化药物偶联物(FeADC),可在肿瘤细胞中实现有效的MAPK阻断,并具有优越的全身耐受性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Potent human broadly SARS-CoV-2-neutralizing IgA and IgG antibodies effective against Omicron BA.1 and BA.2. DCs at the center of help: Origins and evolution of the three-cell-type hypothesis. Chemokines form nanoparticles with DNA and can superinduce TLR-driven immune inflammation. Intestinal toxicity to CTLA-4 blockade driven by IL-6 and myeloid infiltration CCL17 acts as a novel therapeutic target in pathological cardiac hypertrophy and heart failure
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1