Abstract
Aberrant Kras signaling is observed in a high percentage of human lung cancers while activating mutations in the Wnt/b-catenin signaling pathway are only rarely found. Our recent work has shown that the combined activation of both Kras and Wnt/b-catenin signaling leads to a dramatic increase in both tumor incidence and size. Moreover, lung tumors generated by the combined activation of both of these pathways exhibit a distinct phenotype similar to embryonic progenitors found in the developing lung. Thus, combinatorial activation of Kras and Wnt/b-catenin pathways leads to a significant increase in lung tumor formation characterized by a more progenitor like phenotype.