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.
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.
|Razidlo, Gina L; Burton, Kevin M; McNiven, Mark A (2018) Interleukin-6 promotes pancreatic cancer cell migration by rapidly activating the small GTPase CDC42. J Biol Chem 293:11143-11153|
|Chaker, Mahmoud; Minden, Audrey; Chen, Suzie et al. (2018) Rho GTPase effectors and NAD metabolism in cancer immune suppression. Expert Opin Ther Targets 22:9-17|
|Sugimoto, Motokazu; Farnell, Michael B; Nagorney, David M et al. (2018) Decreased Skeletal Muscle Volume Is a Predictive Factor for Poorer Survival in Patients Undergoing Surgical Resection for Pancreatic Ductal Adenocarcinoma. J Gastrointest Surg 22:831-839|
|Danai, Laura V; Babic, Ana; Rosenthal, Michael H et al. (2018) Altered exocrine function can drive adipose wasting in early pancreatic cancer. Nature 558:600-604|
|Paradise, Brooke D; Barham, Whitney; Fernandez-Zapico, Martín E (2018) Targeting Epigenetic Aberrations in Pancreatic Cancer, a New Path to Improve Patient Outcomes? Cancers (Basel) 10:|
|Hogan, Kelly A; Cho, Dong Seong; Arneson, Paige C et al. (2018) Tumor-derived cytokines impair myogenesis and alter the skeletal muscle immune microenvironment. Cytokine 107:9-17|
|Tarragó, Mariana G; Chini, Claudia C S; Kanamori, Karina S et al. (2018) A Potent and Specific CD38 Inhibitor Ameliorates Age-Related Metabolic Dysfunction by Reversing Tissue NAD+ Decline. Cell Metab 27:1081-1095.e10|
|Chini, Eduardo N; Chini, Claudia C S; Espindola Netto, Jair Machado et al. (2018) The Pharmacology of CD38/NADase: An Emerging Target in Cancer and Diseases of Aging. Trends Pharmacol Sci 39:424-436|
|Antwi, Samuel O; Bamlet, William R; Pedersen, Katrina S et al. (2018) Pancreatic Cancer Risk is Modulated by Inflammatory Potential of Diet and ABO Genotype: A Consortia-based Evaluation and Replication Study. Carcinogenesis :|
|Klein, Alison P; Wolpin, Brian M; Risch, Harvey A et al. (2018) Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer. Nat Commun 9:556|
Showing the most recent 10 out of 336 publications