Objective To establish a spontaneous pulmonary tumor mouse model in which the K-Ｒas gene was activated by Cre /loxp recombinant enzyme system． Methods SPC-CＲE transgenic mice were generated that lowly express lung-specific Cre recombinant enzyme． The SPC-CＲE transgenic mice were mated with LSL K-ras G12D transgenic mice to produce SPC-CＲE-Kras double transgenic mice． The 4，5，7 and 9 month-old SPC-CＲE-Kras double transgenic mice were sacrificed and the lung tissues were extracted，fixed，embedded in paraffin and sliced． Hematoxylin-eosin ( HE) staining was performed and observed under light microscope． Micro-CT was used to test the pulmonary nodules of SPC-CＲE-Kras double transgenic mice． Ｒesults The SPC-CＲE-Kras double transgenic mice were generated． The expression of K-ras G12D in the SPC-CＲE-Kras double transgenic mice could be induced by the Cre /Loxp recombinant enzyme system． Mild pulmonary inflammation could be found in the 4 month-old SPC-CＲE-Kras double transgenic mice． The sporadic adenoma could be found in the lung of 5 month-old mice，with 100% of the mice developing pulmonary adenoma ( female 6 /6，male 6 /6) ． The size and progression of the adenoma is time dependent． The pulmonary nodules could be determined by microCT in the 9 month-old． Conclusions A chronic spontaneous pulmonary tumor mouse model was established by hybridization． Longer progressive period from inflammation to adenoma in this model will provide enough time for the investigation of pulmonary tumorigenesis．