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De novo lipogenesis represents a therapeutic target in Kras mutant NSCLC

ABSTRACT: 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.

INSTRUMENT(S): [MoGene-1_0-st] Affymetrix Mouse Gene 1.0 ST Array [transcript (gene) version]

SUBMITTER: George Acquaah-Mensah  

PROVIDER: GSE113717 | GEO | 2018-04-27


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Oncogenic Kras mutations are one of the most common alterations in non-small cell lung cancer and are associated with poor response to treatment and reduced survival. Driver oncogenes, such as Kras are now appreciated for their ability to promote tumor growth via up-regulation of anabolic pathways. Therefore, we wanted to identify metabolic vulnerabilities in Kras-mutant lung cancer. Using the Kras LSL-G12D lung cancer model, we show that mutant Kras drives a lipogenic gene-expression program. S  ...[more]

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