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Publication : Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene.

First Author  Meuwissen R Year  2001
Journal  Oncogene Volume  20
Issue  45 Pages  6551-8
PubMed ID  11641780 Mgi Jnum  J:72206
Mgi Id  MGI:2151994 Doi  10.1038/sj.onc.1204837
Citation  Meuwissen R, et al. (2001) Mouse model for lung tumorigenesis through Cre/lox controlled sporadic activation of the K-Ras oncogene. Oncogene 20(45):6551-8
abstractText  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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