Alejandro Sweet-Cordero

Publication Details

  • Requirement for Rac1 in a K-ras-induced lung cancer in the mouse CANCER RESEARCH Kissil, J. L., Walmsley, M. J., Hanlon, L., Haigis, K. M., Kim, C. F., Sweet-Cordero, A., Eckman, M. S., Tuveson, D. A., Capobianco, A. J., Tybulewicz, V. L., Jacks, T. 2007; 67 (17): 8089-8094


    Given the prevalence of Ras mutations in human cancer, it is critical to understand the effector pathways downstream of oncogenic Ras leading to transformation. To directly assess the requirement for Rac1 in K-ras-induced tumorigenesis, we employed a model of lung cancer in which an oncogenic allele of K-ras could be activated by Cre-mediated recombination in the presence or absence of conditional deletion of Rac1. We show that Rac1 function is required for tumorigenesis in this model. Furthermore, although Rac1 deletion alone was compatible with cell viability and proliferation, when combined with K-ras activation in primary epithelial cells, loss of Rac1 caused a profound reduction in proliferation. These data show a specific requirement for Rac1 function in cells expressing oncogenic K-ras.

    View details for DOI 10.1158/0008-5472.CAN-07-2300

    View details for Web of Science ID 000249406700024

    View details for PubMedID 17804720

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