类有机物
同基因
静脉注射
癌变
结直肠癌
癌症研究
生物
体内
转移
癌症
上皮-间质转换
病理
医学
遗传学
作者
Atsuya Morita,Mizuho Nakayama,Hiroko Oshima,Masanobu Oshima
出处
期刊:Methods in molecular biology
日期:2023-01-01
卷期号:: 19-30
标识
DOI:10.1007/978-1-0716-3331-1_2
摘要
It has been established that the accumulation of driver gene mutations causes malignant progression of colorectal cancer (CRC) through positive selection and clonal expansion, similar to Darwin’s evolution. Following this multistep tumorigenesis concept, we previously showed the specific mutation patterns for each process of malignant progression, including submucosal invasion, epithelial mesenchymal transition (EMT), intravasation, and metastasis, using genetically engineered mouse and organoid models. However, we also found that certain populations of cancer-derived organoid cells lost malignant characteristics of metastatic ability, although driver mutations were not impaired, and such subpopulations were eliminated from the tumor tissues by negative selection. These organoid model studies have contributed to our understanding of the cancer evolution mechanism. We herein report the in vitro and in vivo experimental protocols to investigate the survival, growth, and metastatic ability of intestinal tumor-derived organoids. The model system will be useful for basic research as well as the development of clinical strategies.
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