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.
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.
|Liou, Geou-Yarh; Döppler, Heike; Necela, Brian et al. (2015) Mutant KRAS-induced expression of ICAM-1 in pancreatic acinar cells causes attraction of macrophages to expedite the formation of precancerous lesions. Cancer Discov 5:52-63|
|Young, Steven H; Rey, Osvaldo; Sinnett-Smith, James et al. (2014) Intracellular Ca2+ oscillations generated via the Ca2+-sensing receptor are mediated by negative feedback by PKC? at Thr888. Am J Physiol Cell Physiol 306:C298-306|
|Sinnett-Smith, James; Ni, Yang; Wang, Jia et al. (2014) Protein kinase D1 mediates class IIa histone deacetylase phosphorylation and nuclear extrusion in intestinal epithelial cells: role in mitogenic signaling. Am J Physiol Cell Physiol 306:C961-71|
|Lu, Qing-Yi; Zhang, Lifeng; Eibl, Guido et al. (2014) Overestimation of flavonoid aglycones as a result of the ex vivo deconjugation of glucuronides by the tissue *-glucuronidase. J Pharm Biomed Anal 88:364-9|
|Arensman, Michael D; Telesca, Donatello; Lay, Anna R et al. (2014) The CREB-binding protein inhibitor ICG-001 suppresses pancreatic cancer growth. Mol Cancer Ther 13:2303-14|
|Kong, Ming; Zhu, Longdong; Bai, Li et al. (2014) Vitamin D deficiency promotes nonalcoholic steatohepatitis through impaired enterohepatic circulation in animal model. Am J Physiol Gastrointest Liver Physiol 307:G883-93|
|Rozengurt, Enrique; Soares, Heloisa P; Sinnet-Smith, James (2014) Suppression of feedback loops mediated by PI3K/mTOR induces multiple overactivation of compensatory pathways: an unintended consequence leading to drug resistance. Mol Cancer Ther 13:2477-88|
|Ming, Ming; Sinnett-Smith, James; Wang, Jia et al. (2014) Dose-Dependent AMPK-Dependent and Independent Mechanisms of Berberine and Metformin Inhibition of mTORC1, ERK, DNA Synthesis and Proliferation in Pancreatic Cancer Cells. PLoS One 9:e114573|
|Edderkaoui, Mouad; Eibl, Guido (2014) Risk factors for pancreatic cancer: underlying mechanisms and potential targets. Front Physiol 5:490|
|Soares, Heloisa P; Ni, Yang; Kisfalvi, Krisztina et al. (2013) Different patterns of Akt and ERK feedback activation in response to rapamycin, active-site mTOR inhibitors and metformin in pancreatic cancer cells. PLoS One 8:e57289|
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