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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA117969-09
Application #
8603775
Study Section
Special Emphasis Panel (ZCA1-RPRB-0)
Project Start
Project End
Budget Start
2014-01-01
Budget End
2014-12-31
Support Year
9
Fiscal Year
2014
Total Cost
$121,147
Indirect Cost
Name
University of Texas MD Anderson Cancer Center
Department
Type
DUNS #
800772139
City
Houston
State
TX
Country
United States
Zip Code
77030
Lundquist, Mark R; Goncalves, Marcus D; Loughran, Ryan M et al. (2018) Phosphatidylinositol-5-Phosphate 4-Kinases Regulate Cellular Lipid Metabolism By Facilitating Autophagy. Mol Cell 70:531-544.e9
Hopkins, Benjamin D; Pauli, Chantal; Du, Xing et al. (2018) Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature 560:499-503
Biancur, Douglas E; Kimmelman, Alec C (2018) The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance. Biochim Biophys Acta Rev Cancer 1870:67-75
Chen, Yang; LeBleu, Valerie S; Carstens, Julienne L et al. (2018) Dual reporter genetic mouse models of pancreatic cancer identify an epithelial-to-mesenchymal transition-independent metastasis program. EMBO Mol Med 10:
Hill, Margaret A; Alexander, William B; Guo, Bing et al. (2018) Kras and Tp53 Mutations Cause Cholangiocyte- and Hepatocyte-Derived Cholangiocarcinoma. Cancer Res 78:4445-4451
Mendt, Mayela; Kamerkar, Sushrut; Sugimoto, Hikaru et al. (2018) Generation and testing of clinical-grade exosomes for pancreatic cancer. JCI Insight 3:
Patra, Krushna C; Kato, Yasutaka; Mizukami, Yusuke et al. (2018) Mutant GNAS drives pancreatic tumourigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism. Nat Cell Biol 20:811-822
Anglin, Justin; Zavareh, Reza Beheshti; Sander, Philipp N et al. (2018) Discovery and optimization of aspartate aminotransferase 1 inhibitors to target redox balance in pancreatic ductal adenocarcinoma. Bioorg Med Chem Lett 28:2675-2678
Yang, Annan; Herter-Sprie, Grit; Zhang, Haikuo et al. (2018) Autophagy Sustains Pancreatic Cancer Growth through Both Cell-Autonomous and Nonautonomous Mechanisms. Cancer Discov 8:276-287
Santana-Codina, Naiara; Roeth, Anjali A; Zhang, Yi et al. (2018) Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis. Nat Commun 9:4945

Showing the most recent 10 out of 134 publications