期刊
ONCOGENE
卷 20, 期 45, 页码 6551-6558出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1204837
关键词
somatic activation; Cre-lox; conditional K-Ras allele; lung epithelial tissue; lung tumors; non-small cell lung cancer
The onset of human lung cancer occurs through sequential mutations in oncogenes and tumor suppressor genes. Mutations in K-Ras play a prominent role in human non-small cell lung cancer. We have developed a mouse lung tumor model in which K-Ras can be sporadically activated through Cre-lox mediated somatic recombination. Adenoviral mediated delivery of Cre recombinase in lung epithelial cells gave rise to rapid onset of tumorigenesis, yielding pulmonary adenocarcinomas with 100% incidence after a short latency. The lung tumor lesions shared many features with human non-small cell lung cancer. Our data show that sporadic expression of the K-Ras oncogene is sufficient to elicit lung tumorigenesis. Therefore this model has many advantages over conventional transgenic models used thus far.
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