Activating point mutations of the mouse Kras2 oncogene or its human homologue, KRAS, are critical for lung adenocarcinoma genesis, independent of the species. Significantly, in the mouse, several polymorphic Kras2 alleles have been identified, which cosegregate with genetic susceptibility to chemical induction of lung tumors. Moreover, a major lung tumor susceptibility locus, the Pas1 (Pulmonary adenoma susceptibility 1), was found to colocalize with Kras2 on distal chromosome 6 on linkage analysis. The Kras2 may thus be involved in both cellular transformation and genetic control of tumor susceptibility. In this review, the focus is on current knowledge regarding the relationship between Kras2 and experimental mouse lung carcinogenesis, especially from the aspect of disease predisposition. Because mouse and human lung tumors share considerable similarities, the experimental information should provide clues to personalized medicine in the human setting.
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