The overall purpose of the Animal Models Core (Core D) is to facilitate the accomplishment of the translational research goals and objectives of the SPORE by providing investigators with assistance in the design and generation of transgenic and knockout/knockin mouse strains, a centralized repository for these mouse strains, and material of common interest, such as dissected tissues, DNA, RNA, or protein extracts from these mouse strains.
The specific aims of the Animal Models Core are to: 1. Generate and provide transgenic and knockout/knockin mouse strains as needed by SPORE investigators. 2. Serve as a centralized repository and breeding service for mouse strains used by SPORE investigators. 3. Provide SPORE laboratories with dissected tissues, DNA, RNA, and proteins from the mouse mutants utilized by the investigators. With the recent establishment of a standardized preclinical trial protocol developed by our Core and based on phase II and III patient clinical trials, we anticipate further increased use of our Core by members of our SPORE.
The Animal Models Core is an essential component of our SPORE in Prostate Cancer because it facilitates the timely conduct of research by centralizing services designed to prioritize the needs of our SPORE investigators: maintaining colonies of mice ready for use in preclinical studies and procuring and banking tissue from these mice for characterization of molecular markers and for RNA, DNA, and protein studies.
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|Bose, Rohit; Karthaus, Wouter R; Armenia, Joshua et al. (2017) ERF mutations reveal a balance of ETS factors controlling prostate oncogenesis. Nature 546:671-675|
|Yang, Zhaohui; Peng, Yu-Ching; Gopalan, Anuradha et al. (2017) Stromal hedgehog signaling maintains smooth muscle and hampers micro-invasive prostate cancer. Dis Model Mech 10:39-52|
|O'Rourke, Kevin P; Loizou, Evangelia; Livshits, Geulah et al. (2017) Transplantation of engineered organoids enables rapid generation of metastatic mouse models of colorectal cancer. Nat Biotechnol 35:577-582|
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|Blattner, Mirjam; Liu, Deli; Robinson, Brian D et al. (2017) SPOP Mutation Drives Prostate Tumorigenesis In Vivo through Coordinate Regulation of PI3K/mTOR and AR Signaling. Cancer Cell 31:436-451|
|Vickers, Andrew J; Van Calster, Ben; Steyerberg, Ewout (2017) Decision Curves, Calibration, and Subgroups. J Clin Oncol 35:472-473|
|Hyman, David M; Smyth, Lillian M; Donoghue, Mark T A et al. (2017) AKT Inhibition in Solid Tumors With AKT1 Mutations. J Clin Oncol 35:2251-2259|
|Zhang, Pingzhao; Wang, Dejie; Zhao, Yu et al. (2017) Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation. Nat Med 23:1055-1062|
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