Generation of genetically engineered mice for lung cancer with mutant EGFR

T790米 奥西默替尼 荧光素酶 癌症研究 转基因 突变体 表皮生长因子受体 基因靶向 生物 转基因小鼠 吉非替尼 癌变 体内 癌症 基因 埃罗替尼 遗传学 转染
作者
Dasom Kim,Wonjun Ji,Dong Ha Kim,Yun Jung Choi,Kyungtaek Im,Chae Won Lee,Jeongin Cho,Joongkee Min,Dong‐Cheol Woo,Chang‐Min Choi,Jae Cheol Lee,Young Hoon Sung,Jin Kyung Rho
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier BV]
卷期号:632: 85-91 被引量:1
标识
DOI:10.1016/j.bbrc.2022.09.104
摘要

Although epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) have shown dramatic response and improvement in treating lung cancer with mutant EGFR, the emergence of drug resistance remains a major problem. In particular, some mutations including T790 M and C797S have been recognized as mechanisms of acquired resistance because they weaken binding affinity to drugs. To date, many attempts have been made to develop a new drug for overcoming acquired resistance to EGFR-TKIs, including secondary mutations. However, an appropriate animal model to evaluate in vivo efficacy during novel drug development remains lacking. In this study, we generated a novel transgenic mouse model that conditionally expresses human EGFRL858R/T790M/C797S and firefly luciferase using Cas9-mediated homology-independent targeted integration. Using a lung-specific Sftpc-CreERT2 mouse line, we induced expression of both the human EGFRL858R/T790M/C797S transgene and firefly luciferase in the lungs of adult mice. The expression of these genes and lung cancer occurrence was monitored using an in vivo imaging system and magnetic resonance imaging, respectively. Overall, our mouse model can be utilized to develop new drugs for overcoming C797S-mediated resistance to osimertinib; further, such knock-in systems for expressing oncogenes may be applied to study tumorigenesis and the development of other targeted agents.
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