Overview of the Resource. Given the inherent difficulties in obtaining large quantities of tissues from pancreatic cancer patients, we have devised and instituted a rapid autopsy program that is designed to harvest primary tumor and organs containing all metastatic deposits of tumor from individuals who die of pancreatic cancer. The process we have instituted allows us to harvest and rapidly freeze these tissues in a process that is completed within 5 hours of death. This process is unique and highly innovative as a tissue resource in that it allows us to capture the entire history disease progression for pancreatic cancer patients (from intact primary tumor and remaining precursor lesions through to distant metastases at all locations). For the purposes of this application, the resource will provide high quality frozen samples, slides for frozen sections, formalin fixed tissues, and associated body fluids (blood, serum, ascites) for all projects requiring tissues. The costs of acquiring these tissues in the rapid autopsy program are supported in part by our Cancer Center Support Grant and our Pancreatic Cancer SPORE Grant. The costs requested here are supplemental to that support and are required for the requisite sample processing and pathology support that is associated with supporting the projects proposed in this application.

Agency
National Institute of Health (NIH)
Type
Specialized Center--Cooperative Agreements (U54)
Project #
5U54CA163120-04
Application #
8711375
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
Budget End
Support Year
4
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of Nebraska Medical Center
Department
Type
DUNS #
City
Omaha
State
NE
Country
United States
Zip Code
68198
Hanson, Ryan L; Brown, Roger B; Steele, Maria M et al. (2016) Identification of FRA-1 as a novel player in pancreatic cancer in cooperation with a MUC1: ERK signaling axis. Oncotarget 7:39996-40011
Pai, Priya; Rachagani, Satyanarayana; Dhawan, Punita et al. (2016) MUC4 is negatively regulated through the Wnt/β-catenin pathway via the Notch effector Hath1 in colorectal cancer. Genes Cancer 7:154-68
Muniyan, Sakthivel; Haridas, Dhanya; Chugh, Seema et al. (2016) MUC16 contributes to the metastasis of pancreatic ductal adenocarcinoma through focal adhesion mediated signaling mechanism. Genes Cancer 7:110-24
Huang, Huocong; Svoboda, Robert A; Lazenby, Audrey J et al. (2016) Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1. J Biol Chem 291:23208-23223
Clausen, Thomas Mandel; Pereira, Marina Ayres; Al Nakouzi, Nader et al. (2016) Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility. Mol Cancer Res 14:1288-1299
Joshi, Suhasini; Cruz, Eric; Rachagani, Satyanarayana et al. (2016) Bile acids-mediated overexpression of MUC4 via FAK-dependent c-Jun activation in pancreatic cancer. Mol Oncol 10:1063-77
Pai, Priya; Rachagani, Satyanarayana; Dhawan, Punita et al. (2016) Mucins and Wnt/β-catenin signaling in gastrointestinal cancers: an unholy nexus. Carcinogenesis 37:223-32
Gunda, Venugopal; Yu, Fang; Singh, Pankaj K (2016) Validation of Metabolic Alterations in Microscale Cell Culture Lysates Using Hydrophilic Interaction Liquid Chromatography (HILIC)-Tandem Mass Spectrometry-Based Metabolomics. PLoS One 11:e0154416
Vaz, Arokia Priyanka; Deb, Shonali; Rachagani, Satyanarayana et al. (2016) Overexpression of PD2 leads to increased tumorigenicity and metastasis in pancreatic ductal adenocarcinoma. Oncotarget 7:3317-31
Hein, Ashley L; Seshacharyulu, Parthasarathy; Rachagani, Satyanarayana et al. (2016) PR55α Subunit of Protein Phosphatase 2A Supports the Tumorigenic and Metastatic Potential of Pancreatic Cancer Cells by Sustaining Hyperactive Oncogenic Signaling. Cancer Res 76:2243-53

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