The Mayo Clinic SPORE in Pancreatic Cancer Research will continue to make every effort to maximize the number of innovative and high-quality projects in the Developmental Research Program (DRP). The goal of the DRP is to support innovative, scientifically sound research projects from which findings can be translated into clinically relevant applications that will impact screening, diagnosis, and management of pancreatic cancer. Progress from Years 05 to 10 has resulted in support for 26 of 64 (41%) DRP applications. These meritorious projects have yielded important new insights about pancreatic cancer and have led to extramural funding, including contributions to the full translational research projects in this current SPORE application.
The Specific Aims of the DRP are to: (1) Encourage and solicit innovative translationally-relevant laboratory, population and clinical study proposals and support interdisciplinary collaboration in translational research in pancreatic cancer;(2) Conduct a thorough evaluation of all applications for the DRP award;(3) Evaluate and monitor progress of DRP awardees;and (4) Facilitate opportunities for extramural funding and integration into future SPORE projects. These projects will generate new hypotheses that can be tested in larger-scale research projects or clinical trials that can impact pancreatic cancer. The DRP will provide up to $50,000 (utilizing funds from both the SPORE grant and institutional resources) to 2 to 3 projects annually. There will be the possibility of a second year of support based on progress. A successfully established process will call for applications on an annual basis and to formally peer review submissions utilizing the expertise of the Scientific Advisory Committee and others as needed, including our Advocates. Criteria will be based upon scientific merit, originality, qualifications of the key personnel and interactions, and translational potential. It is the intent of the SPORE leadership to encourage and help the investigators to use the data generated by these projects to design either R01-type grants or similar extramural proposals in the next funding period.
The Developmental Research Program is a very important resource for innovative research in pancreatic cancer. A rigorous process ensures transparency and fair review of applications. Scientific merit, originality, and potential for translation are key criteria for selecting two to three applications each year.
|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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