Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene
Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene
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DOI：
10.1038/sj.onc.1204837
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发表时间：
2001-10-04
期刊：
影响因子：
8
通讯作者：
Berns, A
中科院分区：
文献类型：
--
作者：
Meuwissen, R;Linn, SC;Berns, A
人类肺癌的发生是通过癌基因和肿瘤抑制基因的顺序突变而发生的。K-Ras突变在人类非小细胞肺癌中发挥重要作用。我们已经开发了一种小鼠肺肿瘤模型，其中K-Ras可以通过Cre-lox介导的体细胞重组零星激活。腺病毒介导的Cre重组酶在肺上皮细胞中的递送引起肿瘤发生的快速发作，在短潜伏期后产生具有100%发病率的肺腺癌。肺肿瘤病变与人类非小细胞肺癌有许多共同特征。我们的数据表明，K-Ras癌基因的零星表达足以引起肺肿瘤的发生。因此，该模型与迄今为止使用的常规转基因模型相比具有许多优点。
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.