De novo lipogenesis represents a therapeutic target in Kras mutant NSCLC. De novo lipogenesis represents a therapeutic target in Kras mutant NSCLC

We examine the potential of Kras as a metabolic target in lung cancer using the KrasLSL-G12D lung cancer model. We demonstrate that mutant Kras drives a lipogenic gene expression program, and that fatty acid synthesis is important in Kras-induced tumorigenesis. Compare gene expression changes between mutant Kras (G12D) driven lung tumors and normal lung samples to identify pathways selectively altered in lung tumors. Overall design: To identify the pathways selectively modulated by oncogenic Kras (G12D) signaling in lung tumors, we used the transgenic Kras LSL-G12D model of lung cancer. By crossing these mice with another transgenic mice (CC10_Cre) expressing Cre recombinase selectively in Clara cells of the lung, we generated Kras LSL-G12D CC10-Cre mice which selectively express mutant kras in clara cells. These mice develop lung adenocarcinoma and have a median survival of 80 days.