Abstract
Abstract Pancreatic cancer remains the 4th deadliest cancer in the United States in 2009. The 5-year survival rate for all stages remains at 5%, the lowest rate among major malignancies. Lack of methods for early detection, as well as ineffective treatments, contribute to the poor outcome of the disease. Over 90% of the pancreatic cancers are pancreatic ductal adenocarcinomas (PDACs). Mutations in the KRAS gene were found in majority of the PDAC lesions and played critical role in the initiation of tumorigenesis as demonstrated in transgenic mouse models. Recent pancreatic cancer genome sequencing results have highlighted the major pathways that can be altered in PDACs. The study also produced a list of novel oncogene candidates that may play parts in the rise of pancreatic cancer. To facilitate the evaluation of these candidate oncogenes’ function in pancreatic cancer in vivo, we developed zebrafish models that can overexpress transgenes specifically in pancreas, alone or in the presence of a human KRAS mutant transgene. The transgenes were introduced into zebrafish via Tol2 transposon elements. The Gal4/UAS transcriptional regulatory system was utilized to ensure targeted expressions of multiple transgenes in the pancreas, controlled by the regulatory element of the Ptf1a gene, a transcription factor critical for pancreas development. Pancreas-specific expression of the mutant KRAS transgene alone in zebrafish can give rise to pancreatic cancers similar to those observed in humans. We now have the opportunity to functionally assess a wide variety of genetic lesions for their ability to modify pancreatic cancer initiation and/or progression, achieving a level of throughput not technically feasible in the mouse. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4162.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
