The Mayo Clinic SPORE in Pancreatic Cancer has built a robust environment to facilitate high quality research by our talented investigators. Our goal is to apply innovative technologies and resources in basic/clinical/population research to achieve the best strategies for prevention, early detection and therapy and increase survival of this devastating malignancy. The SPORE aims to: 1) Provide the scientific leadership and organization to sustain and support outstanding translational pancreatic cancer (PC) research;2) Provide the organizational infrastructure to facilitate communication and promote interactions among SPORE investigators and the larger research community;3) Provide resources to develop innovative research projects in translational PC research;4) Foster career development in translational PC research;and 5) Assure excellence of research through a rigorous internal review process of the SPORE research programs and projects, with periodic review and support from a panel of outstanding external advisors. We have developed a responsive infrastructure that has spawned innovative research and interdisciplinary interactions, attracting committed investigators. Mayo Clinic sees -725 PC patients yearly, constituting 1.7% of all PC cases in the US. Four cores (Administrative, Biostatistics, Clinical Research, and Tissue) will provide support. Project 1 (new) will identify NFATs and NFAT-dependent target genes and roles, and conduct a Phase I study using cyclosporine A and gemcitabine-abraxane. Project 2 (new) will establish the role of NAD in PC, and use small molecule SIRT1 activating compounds in preclinical studies as well as a Phase I trial using SRT3025 with gemcitabine and abraxane. Project 3 (continuing) will use pursue findings that activation of innate immunity and chemotherapy can synergize curatively against pancreatic cancer, perform Phase l-ll trials which combines the TLRS agonist VentiRx-2337 with cyclophosphamide as second line therapy after FOLFIRINOX, optimizing a vaccine against PC-associated MUC1. Project 4 (new) will identify roles of DNA repair in PC and target patients with double-stranded DNA repair defects for individualized treatment in a Phase II study of the PARP inhibitor rucaparib in chemotherapy refractive PC.

Public Health Relevance

The Mayo Clinic SPORE in Pancreatic Cancer provides a highly supportive environment to foster translational research. Four innovative research projects, pilot awards, and career development awards will be enabled by resources of biostatistics, tissue, and clinical research cores. The ultimate goal is to apply research findings toward prevention, early detection, and therapy to improve survival of pancreatic cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
2P50CA102701-11A1
Application #
8738910
Study Section
Special Emphasis Panel (ZCA1-RPRB-0 (M1))
Program Officer
Agarwal, Rajeev K
Project Start
2014-09-18
Project End
2019-08-31
Budget Start
2014-09-18
Budget End
2015-08-31
Support Year
11
Fiscal Year
2014
Total Cost
$2,162,000
Indirect Cost
$695,066
Name
Mayo Clinic, Rochester
Department
Type
DUNS #
006471700
City
Rochester
State
MN
Country
United States
Zip Code
55905
Chini, Claudia C S; Espindola-Netto, Jair M; Mondal, Gourish et al. (2016) SIRT1-Activating Compounds (STAC) Negatively Regulate Pancreatic Cancer Cell Growth and Viability Through a SIRT1 Lysosomal-Dependent Pathway. Clin Cancer Res 22:2496-507
Murphy, Stephen J; Hart, Steven N; Halling, Geoffrey C et al. (2016) Integrated Genomic Analysis of Pancreatic Ductal Adenocarcinomas Reveals Genomic Rearrangement Events as Significant Drivers of Disease. Cancer Res 76:749-61
Chaiteerakij, Roongruedee; Petersen, Gloria M; Bamlet, William R et al. (2016) Metformin Use and Survival of Patients With Pancreatic Cancer: A Cautionary Lesson. J Clin Oncol 34:1898-904
Cao, H; Eppinga, R D; Razidlo, G L et al. (2016) Stromal fibroblasts facilitate cancer cell invasion by a novel invadopodia-independent matrix degradation process. Oncogene 35:1099-110
Hu, Chunling; Hart, Steven N; Bamlet, William R et al. (2016) Prevalence of Pathogenic Mutations in Cancer Predisposition Genes among Pancreatic Cancer Patients. Cancer Epidemiol Biomarkers Prev 25:207-11
McWilliams, Robert R; Maisonneuve, Patrick; Bamlet, William R et al. (2016) Risk Factors for Early-Onset and Very-Early-Onset Pancreatic Adenocarcinoma: A Pancreatic Cancer Case-Control Consortium (PanC4) Analysis. Pancreas 45:311-6
Carr, Ryan M; Fernandez-Zapico, Martin E (2016) Pancreatic cancer microenvironment, to target or not to target? EMBO Mol Med 8:80-2
Wang, Jianbo; Galvao, Joana; Beach, Krista M et al. (2016) Novel Roles and Mechanism for Krüppel-like Factor 16 (KLF16) Regulation of Neurite Outgrowth and Ephrin Receptor A5 (EphA5) Expression in Retinal Ganglion Cells. J Biol Chem 291:18084-95
Lopez, Angelica P; Kugelman, Jeffrey R; Garcia-Rivera, Jose et al. (2016) The Structure-Specific Recognition Protein 1 Associates with Lens Epithelium-Derived Growth Factor Proteins and Modulates HIV-1 Replication. J Mol Biol 428:2814-31
Lakshminarayanan, Vani; Supekar, Nitin T; Wei, Jie et al. (2016) MUC1 Vaccines, Comprised of Glycosylated or Non-Glycosylated Peptides or Tumor-Derived MUC1, Can Circumvent Immunoediting to Control Tumor Growth in MUC1 Transgenic Mice. PLoS One 11:e0145920

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