Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 신윤용 | * |
dc.contributor.author | 김대기 | * |
dc.date.accessioned | 2016-08-27T04:08:50Z | - |
dc.date.available | 2016-08-27T04:08:50Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 1347-9032 | * |
dc.identifier.issn | 1349-7006 | * |
dc.identifier.other | OAK-16397 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/218005 | - |
dc.description.abstract | Recent strategies for treating CML patients have focused on investigating new combinations of tyrosine kinase inhibitors (TKIs) as well as identifying novel translational research agents that can eradicate CML leukemia-initiating cells (CML-LICs). However, little is known about the therapeutic benefits such CML-LIC targeting therapies might bring to CML patients. In this study, we investigated the therapeutic potential of EW-7197, an orally bioavailable transforming growth factor- signaling inhibitor which has recently been approved as an Investigational New Drug (NIH, USA), to suppress CML-LICs in vivo. Compared to TKI treatment alone, administration of TKI plus EW-7197 to CML-affected mice significantly delayed disease relapse and prolonged survival. Notably, combined treatment with EW-7197 plus TKI was effective in eliminating CML-LICs even if they expressed the TKI-resistant T315I mutant BCR-ABL1 oncogene. Collectively, these results indicate that EW-7197 may be a promising candidate for a new therapeutic that can greatly benefit CML patients by working in combination with TKIs to eradicate CML-LICs. | * |
dc.language | English | * |
dc.publisher | WILEY-BLACKWELL | * |
dc.subject | ALK5 inhibitor | * |
dc.subject | CML stem cells | * |
dc.subject | relapse prevention | * |
dc.subject | TGF- signaling | * |
dc.subject | TKI resistance | * |
dc.title | Novel oral transforming growth factor- signaling inhibitor EW-7197 eradicates CML-initiating cells | * |
dc.type | Article | * |
dc.relation.issue | 2 | * |
dc.relation.volume | 107 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 140 | * |
dc.relation.lastpage | 148 | * |
dc.relation.journaltitle | CANCER SCIENCE | * |
dc.identifier.doi | 10.1111/cas.12849 | * |
dc.identifier.wosid | WOS:000371484100005 | * |
dc.identifier.scopusid | 2-s2.0-84958923762 | * |
dc.author.google | Naka, Kazuhito | * |
dc.author.google | Ishihara, Kaori | * |
dc.author.google | Jomen, Yoshie | * |
dc.author.google | Jin, Cheng Hua | * |
dc.author.google | Kim, Dong-Hyun | * |
dc.author.google | Gu, Yoon-Kang | * |
dc.author.google | Jeong, Eun-Sook | * |
dc.author.google | Li, Shaoguang | * |
dc.author.google | Krause, Daniela S. | * |
dc.author.google | Kim, Dong-Wook | * |
dc.author.google | Bae, Eunjin | * |
dc.author.google | Takihara, Yoshihiro | * |
dc.author.google | Hirao, Atsushi | * |
dc.author.google | Oshima, Hiroko | * |
dc.author.google | Oshima, Masanobu | * |
dc.author.google | Ooshima, Akira | * |
dc.author.google | Sheen, Yhun Yhong | * |
dc.author.google | Kim, Seong-Jin | * |
dc.author.google | Kim, Dae-Kee | * |
dc.contributor.scopusid | 신윤용(6603872711) | * |
dc.contributor.scopusid | 김대기(35083694200) | * |
dc.date.modifydate | 20240118164500 | * |