The BioBank Core will assist project member laboratories in the accrual and centralization of biologic resources that are critically required for pancreatic cancer research. We will take advantage of our immediate access to human surgical specimens to provide P01 investigators with biological materials that have been subjected to extensive characterization at the histologic (in collaboration with the Experimental Pathology Core) and genetic levels. The Core will collect, initiate, maintain, archive and record all human PDAC biologic resources. These materials include serially passaged xenografts created from primary and metastatic human pancreatic cancer specimens and a repository of PDAC cell lines. The xenograft tumors and cell lines have been subjected to high-resolution aCGH and expression profiling, enabling investigators to retrieve needed biologic materials with an appropriate genomic profile. Together, these resources should facilitate molecular studies and provide standardized cellular systems for performing experimental studies. Members of the BioBank Core have extensive experience in implementation of xenograft systems for testing novel therapeutic approaches and for molecular and biological studies. The Core will interact closely with the projects of the P01 to provide the biological materials and aid in the design and interpretation of experiments employing the xenografts and primary cells. The Core will seek to ensure a high level of quality control of specimens and standardization of protocols to ensure the effective translation of results between P01 projects.
Pancreatic cancer is a disease without a cure. One of the major limiting factor is in the study of this disease is access to high-quality tissue samples. The resources provided by the BioBank Core will provide investigators with ample tissues and cell lines critical to the analysis of key molecular pathways that can be targeted to cure pancreatic cancer.
|Kapoor, Avnish; Yao, Wantong; Ying, Haoqiang et al. (2014) Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Cell 158:185-97|
|Sahora, Klaus; Fernández-del Castillo, Carlos; Dong, Fei et al. (2014) Not all mixed-type intraductal papillary mucinous neoplasms behave like main-duct lesions: implications of minimal involvement of the main pancreatic duct. Surgery 156:611-21|
|Mayers, Jared R; Wu, Chen; Clish, Clary B et al. (2014) Elevation of circulating branched-chain amino acids is an early event in human pancreatic adenocarcinoma development. Nat Med 20:1193-8|
|Lee, John J; Perera, Rushika M; Wang, Huaijun et al. (2014) Stromal response to Hedgehog signaling restrains pancreatic cancer progression. Proc Natl Acad Sci U S A 111:E3091-100|
|Deschênes-Simard, Xavier; Lessard, Frédéric; Gaumont-Leclerc, Marie-France et al. (2014) Cellular senescence and protein degradation: breaking down cancer. Cell Cycle 13:1840-58|
|Daver, Naval; Shastri, Aditi; Kadia, Tapan et al. (2014) Phase II study of pomalidomide in combination with prednisone in patients with myelofibrosis and significant anemia. Leuk Res 38:1126-9|
|Viale, Andrea; Pettazzoni, Piergiorgio; Lyssiotis, Costas A et al. (2014) Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Nature 514:628-32|
|Lyssiotis, Costas A; Cantley, Lewis C (2014) Targeting metabolic scavenging in pancreatic cancer. Clin Cancer Res 20:6-8|
|Commisso, Cosimo; Davidson, Shawn M; Soydaner-Azeloglu, Rengin G et al. (2013) Macropinocytosis of protein is an amino acid supply route in Ras-transformed cells. Nature 497:633-7|
|Lyssiotis, Costas A; Son, Jaekyoung; Cantley, Lewis C et al. (2013) Pancreatic cancers rely on a novel glutamine metabolism pathway to maintain redox balance. Cell Cycle 12:1987-8|
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