The Biospecimen Repository Core is designed to provide support to the basic translational research efforts ofthe SPORE. The Core will play a central role in collecting, annotating, storing, distributing, and tracking prostate cancer tissue and blood biospecimens from patients enrolled in research protocols. Detailed biospecimen annotation, including documentation of preanalytic processing variables, pathology findings, and patient clinical history information will be recorded in robust relational databases. We will conduct rigorous data quality assurance and quality control measures, and standardized longitudinal follow-up of all consented patients with materials in the prostate biospecimen repository. The Core will provide SPORE investigators with expert histopathological evaluation of tumor samples both from patients enrolled on research protocols and from xenograft models. The Core will also provide assistance in performing and interpreting immunohistochemical and in situ hybridization assays, in selecting tissue for microdissection and construction of arrays, and in collaborating with project leaders and the Biostatistics Core.
Specific Aim 1. To maintain and expand a model prostate cancer resource to collect, annotate, store, and distribute biospecimens for translational prostate cancer research.
Specific Aim 2. To perform systematic pathologic evaluation of all human and animal tissue samples and preparation of appropriate tissues for use by SPORE investigators. Furthermore, the Core aims will serve as a focal point to help combine and prioritize a variety of institutional pathology systems-related development efforts, and we plan to document and publish our findings, standard operating procedures, and best practices, to better serve the research community. Core A will serve RP-2, Core D
Through the work of this SPORE, supported by the Biospecimen Repository Core, we hope to increase our understanding of the clinical, biologic, and genetic basis of prostate cancer in an effort to improve patient outcome, to facilitate a range of scientific activities that could lead to new genomic- and proteomic-based interventions for cancer, including target identification and validation, and to develop new biomarkers, diagnostics, and pharmacogenomic analyses.
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|Vertosick, Emily A; Assel, Melissa; Vickers, Andrew J (2017) A systematic review of instrumental variable analyses using geographic region as an instrument. Cancer Epidemiol 51:49-55|
|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|
|Ku, Sheng Yu; Rosario, Spencer; Wang, Yanqing et al. (2017) Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance. Science 355:78-83|
|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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