Somatic activation of the K-ras oncogene causes early onset lung cancer in mice

Leisa Johnson, Kim Mercer, Doron Greenbaum, Roderick T. Bronson, Denise Crowley, David A. Tuveson and Tyler Jacks ()
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Leisa Johnson: Massachusetts Institute of Technology, and
Kim Mercer: Massachusetts Institute of Technology, and
Doron Greenbaum: Massachusetts Institute of Technology, and
Roderick T. Bronson: Tufts University Schools of Medicine and Veterinary Medicine
Denise Crowley: Massachusetts Institute of Technology, and
David A. Tuveson: Massachusetts Institute of Technology, and
Tyler Jacks: Massachusetts Institute of Technology, and

Nature, 2001, vol. 410, issue 6832, 1111-1116

Abstract: Abstract About 30% of human tumours carry ras gene mutations1,2. Of the three genes in this family (composed of K-ras, N-ras and H-ras), K-ras is the most frequently mutated member in human tumours, including adenocarcinomas of the pancreas (∼70–90% incidence), colon (∼50%) and lung (∼25–50%)1,2,3,4,5,6. To constuct mouse tumour models involving K-ras, we used a new gene targeting procedure to create mouse strains carrying oncogenic alleles of K-ras that can be activated only on a spontaneous recombination event in the whole animal. Here we show that mice carrying these mutations were highly predisposed to a range of tumour types, predominantly early onset lung cancer. This model was further characterized by examining the effects of germline mutations in the tumour suppressor gene p53, which is known to be mutated along with K-ras in human tumours. This approach has several advantages over traditional transgenic strategies, including that it more closely recapitulates spontaneous oncogene activation as seen in human cancers.

Date: 2001
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DOI: 10.1038/35074129

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