The Administrative Core will be responsible for overseeing the daily functions of the programs in fulfilling the goal of this program project grant. The Core will provide administrative support, including support for grants and financial management;scheduling of meetings and seminars;coordination of activities between this POI and UCLA academic and administrative bodies, and the VA Greater Los Angeles Healthcare System-West Los Angeles. The Core will also provide biostatistical support for all research projects and the management of research data and shared data function of the program. It will have the responsibility of managing details of the budget, appropriately filing budgetary information, and will file progress reports and communicate with NCI. The scheduling, dissemination of information, and organization of the program project Symposium, including the participation of the External Advisory Board, and oversight all of the established policies for recruitment of women and minorities, and interaction with other NCI programs will also be the responsibilities of the Administrative Core. The Administrative Core, under the direction of Dr. Vay Liang W. Go and Dr. Gang Li will provide biostatistical support: The research projects are: Project 1 investigates the importance of inflammation on diet-induced pancreatic cancer development and explores the role of prostaglandin signaling in this process, Project 2 explores in the intracellular signaling processes that are operative in diet- induced pancreatic cancer development and the efficacy of fish oil (1) and metformin (2) in diet-induced pancreatic cancer development, Project 3 will examine the importance of autophagy, and Project 4 is the role of desmoplasia in diet-induced pancreatic cancer development. All projects are integrated and synergistic and utilize two Cores, an Administrative (Core A) and Animal Core (Core B). The projects will also utilize our shared core, including those at NCCAM funded UCLA Center for Excellence in Pancreatic Diseases, NDDK supported Digestive Disease Core Center, NIAAA funded Southern California Center for Alcohol Liver and Pancreatic Disease, other UCLA shared core resources in fulfilling the program project's goal in targeting diet-induced promotion of Kras-induced pancreatic cancer.

Public Health Relevance

It is the Administrative Core's goal to provide the key management responsibilities to accomplish this program project's goal in investigating the underlying mechanism in vivo animal model, to provide specific translational potential and future projects in the prevention and treatment of pancreatic cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA163200-03
Application #
8712201
Study Section
Special Emphasis Panel (ZCA1-RPRB-B)
Project Start
Project End
Budget Start
2014-08-01
Budget End
2015-07-31
Support Year
3
Fiscal Year
2014
Total Cost
$150,715
Indirect Cost
$72,345
Name
University of California Los Angeles
Department
Type
DUNS #
092530369
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
Eibl, Guido; Cruz-Monserrate, Zobeida; Korc, Murray et al. (2018) Diabetes Mellitus and Obesity as Risk Factors for Pancreatic Cancer. J Acad Nutr Diet 118:555-567
Xu, Mu; Jung, Xiaoman; Hines, O Joe et al. (2018) Obesity and Pancreatic Cancer: Overview of Epidemiology and Potential Prevention by Weight Loss. Pancreas 47:158-162
Zheng, Han; You, Yang; Hua, Meiyun et al. (2018) Chlorophyllin Modulates Gut Microbiota and Inhibits Intestinal Inflammation to Ameliorate Hepatic Fibrosis in Mice. Front Physiol 9:1671
Waldron, Richard T; Su, Hsin-Yuan; Piplani, Honit et al. (2018) Ethanol Induced Disordering of Pancreatic Acinar Cell Endoplasmic Reticulum: An ER Stress/Defective Unfolded Protein Response Model. Cell Mol Gastroenterol Hepatol 5:479-497
Kaur, Kawaljit; Chang, Hui-Hua; Topchyan, Paytsar et al. (2018) Deficiencies in Natural Killer Cell Numbers, Expansion, and Function at the Pre-Neoplastic Stage of Pancreatic Cancer by KRAS Mutation in the Pancreas of Obese Mice. Front Immunol 9:1229
Jin, Yi-Ping; Valenzuela, Nicole M; Zhang, Xiaohai et al. (2018) HLA Class II-Triggered Signaling Cascades Cause Endothelial Cell Proliferation and Migration: Relevance to Antibody-Mediated Transplant Rejection. J Immunol 200:2372-2390
Edderkaoui, Mouad; Chheda, Chintan; Soufi, Badr et al. (2018) An Inhibitor of GSK3B and HDACs Kills Pancreatic Cancer Cells and Slows Pancreatic Tumor Growth and Metastasis in Mice. Gastroenterology 155:1985-1998.e5
Yang, Zemin; Liu, Yu; Qin, Lan et al. (2017) Cathepsin H-Mediated Degradation of HDAC4 for Matrix Metalloproteinase Expression in Hepatic Stellate Cells: Implications of Epigenetic Suppression of Matrix Metalloproteinases in Fibrosis through Stabilization of Class IIa Histone Deacetylases. Am J Pathol 187:781-797
Birtolo, Chiara; Pham, Hung; Morvaridi, Susan et al. (2017) Cadherin-11 Is a Cell Surface Marker Up-Regulated in Activated Pancreatic Stellate Cells and Is Involved in Pancreatic Cancer Cell Migration. Am J Pathol 187:146-155
Lew, Daniel; Afghani, Elham; Pandol, Stephen (2017) Chronic Pancreatitis: Current Status and Challenges for Prevention and Treatment. Dig Dis Sci 62:1702-1712

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