The Clinical Research Core combines the ongoing Patient Registry activities with the new clinical trial activities in all four translational research projects in the proposed funding period.
The aims of the Clinical Research Core are to: 1) perform the necessary clinical trial management support activities;2) centrally coordinate all activities with the infrastructure of the Cancer Center CRO to ensure smooth execution of the SPORE?s early-phase clinical trials;3) perform all patient recruitment activities for the clinical trials in the SPORE projects;4) maintain the ultra-rapid case recruitment and registry of pancreatic cancer patients;and 6) serve as a resource to future Developmental Research Program and Career Developmental Program research projects. The directors of this Core have extensive experience in studies of human subjects and recruitment of patients to research protocols, both for observational studies and clinical trials. Mayo Clinic diagnoses and/or treats an estimated 650 pancreatic cancer patients per year across its three campuses. To date, the pancreatic cancer SPORE?s Patient Registry activities have been very productive, with accrual of 5,395 consented subjects, using ultra-rapid case finding, a necessary method for this rapidly fatal cancer. There are 3,121 pancreatic adenocarcinoma cancer patients in the Registry. In addition, the Registry includes data on over 2,500 age, sex, race, and region-matched healthy controls. It will coordinate its activities very closely with the Biostatistics Core and the Tissue Core to ensure the highest quality annotated biospecimens and pancreatic cancer database for research. The close coordination and oversight of the most senior leaders of the SPORE will ensure that all clinical research activities are performed with the highest level of research integrity and adherence to all human subjects regulations.
The Clinical Research Core has the goal of providing support to SPORE investigators who will perform human studies, including use of biospecimens and data from an ongoing patient registry, and execution of early phase clinical trials. The Core will adhere to the highest standards of integrity and quality and ensure compliance with all regulations and policies that govern human research.
|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 KrÃ¼ppel-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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