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.
|Mullarky, Edouard; Lairson, Luke L; Cantley, Lewis C et al. (2016) A novel small-molecule inhibitor of 3-phosphoglycerate dehydrogenase. Mol Cell Oncol 3:e1164280|
|Saung, May Tun; Sharei, Armon; Adalsteinsson, Viktor A et al. (2016) A Size-Selective Intracellular Delivery Platform. Small :|
|Kugel, Sita; SebastiÃ¡n, Carlos; Fitamant, Julien et al. (2016) SIRT6 Suppresses Pancreatic Cancer through Control of Lin28b. Cell 165:1401-15|
|Sousa, CristovÃ£o M; Biancur, Douglas E; Wang, Xiaoxu et al. (2016) Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion. Nature 536:479-83|
|Mullarky, Edouard; Lucki, Natasha C; Beheshti Zavareh, Reza et al. (2016) Identification of a small molecule inhibitor of 3-phosphoglycerate dehydrogenase to target serine biosynthesis in cancers. Proc Natl Acad Sci U S A 113:1778-83|
|Huang, Yinshi; Nahar, Sabikun; Nakagawa, Akifumi et al. (2016) Regulation of GLI Underlies a Role for BET Bromodomains in Pancreatic Cancer Growth and the Tumor Microenvironment. Clin Cancer Res 22:4259-70|
|Ying, Haoqiang; Dey, Prasenjit; Yao, Wantong et al. (2016) Genetics and biology of pancreatic ductal adenocarcinoma. Genes Dev 30:355-85|
|Dayton, Talya L; Gocheva, Vasilena; Miller, Kathryn M et al. (2016) Germline loss of PKM2 promotes metabolic distress and hepatocellular carcinoma. Genes Dev 30:1020-33|
|Tummala, Krishna S; Kottakis, Filippos; Bardeesy, Nabeel (2016) NRF2: Translating the Redox Code. Trends Mol Med 22:829-831|
|Chakrabarti, Gaurab; Moore, Zachary R; Luo, Xiuquan et al. (2015) Targeting glutamine metabolism sensitizes pancreatic cancer to PARP-driven metabolic catastrophe induced by ÃŸ-lapachone. Cancer Metab 3:12|
Showing the most recent 10 out of 103 publications