Description
Mouse lung cancers were generated using the KrasLA model, in which a latent mutated Kras2 allele (resulting in the amino acid substitution G12D) is sporadically activated through spontaneous homologous recombination. These mice develop lung adenomas with full penetrance; over time, the tumors acquire morphologic characteristics reminiscent of those of human adenocarcinoma, such as nuclear atypia and a high mitotic index.