Kristin Jensen

Publication Details

  • Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma CANCER CELL Kopp, J. L., von Figura, G., Mayes, E., Liu, F., Dubois, C. L., Morris, J. P., Pan, F. C., Akiyama, H., Wright, C. V., Jensen, K., Hebrok, M., Sander, M. 2012; 22 (6): 737-750


    Tumors are largely classified by histologic appearance, yet morphologic features do not necessarily predict cellular origin. To determine the origin of pancreatic ductal adenocarcinoma (PDA), we labeled and traced pancreatic cell populations after induction of a PDA-initiating Kras mutation. Our studies reveal that ductal and stem-like centroacinar cells are surprisingly refractory to oncogenic transformation, whereas acinar cells readily form PDA precursor lesions with ductal features. We show that formation of acinar-derived premalignant lesions depends on ectopic induction of the ductal gene Sox9. Moreover, when concomitantly expressed with oncogenic Kras, Sox9 accelerates formation of premalignant lesions. These results provide insight into the cellular origin of PDA and suggest that its precursors arise via induction of a duct-like state in acinar cells.

    View details for DOI 10.1016/j.ccr.2012.10.025

    View details for Web of Science ID 000312467000007

    View details for PubMedID 23201164

Stanford Medicine Resources:

Footer Links: