Ontology highlight
ABSTRACT: Background
The potential correlation between KIT secondary mutations and Imatinib-resistance in gastrointestinal stromal tumor (GIST) has been hinted, yet their specific linkage and underlying mechanisms remained unelucidated, also the development of substitute strategies dealing with this resistance was urgently needed.Methods
In this study, we explored the distribution of the most prevalent forms of KIT mutation in Chinese GIST patients, after that, we established cell lines that was overexpressed with mutant KIT, and by performing RNA sequencing, immunoblotting and cell viability, we analyzed their functional and mechanistic relevance with Imatinib-resistance in GIST cell lines. Additionally, we evaluated the tumor inhibition efficacy of four regimens in Im
SUBMITTER: Zhao Q
PROVIDER: S-EPMC8748123 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature