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.
|Biancur, Douglas E; Paulo, Joao A; Ma?achowska, Beata et al. (2017) Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism. Nat Commun 8:15965|
|Ravez, Séverine; Corbet, Cyril; Spillier, Quentin et al. (2017) ?-Ketothioamide Derivatives: A Promising Tool to Interrogate Phosphoglycerate Dehydrogenase (PHGDH). J Med Chem 60:1591-1597|
|Nejati, Reza; Goldstein, Jennifer B; Halperin, Daniel M et al. (2017) Prognostic Significance of Tumor-Infiltrating Lymphocytes in Patients With Pancreatic Ductal Adenocarcinoma Treated With Neoadjuvant Chemotherapy. Pancreas 46:1180-1187|
|Cancer Genome Atlas Research Network. Electronic address: email@example.com; Cancer Genome Atlas Research Network (2017) Integrated Genomic Characterization of Pancreatic Ductal Adenocarcinoma. Cancer Cell 32:185-203.e13|
|Lu, Xin; Horner, James W; Paul, Erin et al. (2017) Effective combinatorial immunotherapy for castration-resistant prostate cancer. Nature 543:728-732|
|Lyssiotis, Costas A; Kimmelman, Alec C (2017) Metabolic Interactions in the Tumor Microenvironment. Trends Cell Biol 27:863-875|
|Pergolini, Ilaria; Morales-Oyarvide, Vicente; Mino-Kenudson, Mari et al. (2017) Tumor engraftment in patient-derived xenografts of pancreatic ductal adenocarcinoma is associated with adverse clinicopathological features and poor survival. PLoS One 12:e0182855|
|Sherman, Mara H; Yu, Ruth T; Tseng, Tiffany W et al. (2017) Stromal cues regulate the pancreatic cancer epigenome and metabolome. Proc Natl Acad Sci U S A 114:1129-1134|
|Shukla, Surendra K; Purohit, Vinee; Mehla, Kamiya et al. (2017) MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer. Cancer Cell 32:71-87.e7|
|Dey, Prasenjit; Baddour, Joelle; Muller, Florian et al. (2017) Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer. Nature 542:119-123|
Showing the most recent 10 out of 121 publications