Kras and ciliary gene mutations cooperatively lead to pancreatic tumorigenesis only when induced during embryogenesis.

Mutations in the Kras oncogene are present in approximately 25% of tumors, while defective primary cilium can either promote or suppress specific cancer types. In the present study, we investigated whether mutations in Kras and genes important for primary cilium formation could collaboratively contribute to pancreatic cancer. Using mouse models, we found the presence of collaboration when these mutations were induced in the pancreas during embryogenesis, whereas no collaboration was observed when they were induced after birth. These results help to understand why mutations in ciliary genes do not appear in the mutational landscape of human pancreatic cancer.