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.
|Kim, Jungsun; Bamlet, William R; Oberg, Ann L et al. (2017) Detection of early pancreatic ductal adenocarcinoma with thrombospondin-2 and CA19-9 blood markers. Sci Transl Med 9:|
|Espindola-Netto, Jair Machado; Chini, Claudia C S; Tarragó, Mariana et al. (2017) Preclinical efficacy of the novel competitive NAMPT inhibitor STF-118804 in pancreatic cancer. Oncotarget 8:85054-85067|
|Pathangey, Latha B; McCurry, Dustin B; Gendler, Sandra J et al. (2017) Surrogate in vitro activation of innate immunity synergizes with interleukin-7 to unleash rapid antigen-driven outgrowth of CD4+ and CD8+ human peripheral blood T-cells naturally recognizing MUC1, HER2/neu and other tumor-associated antigens. Oncotarget 8:10785-10808|
|Javeed, Naureen; Mukhopadhyay, Debabrata (2017) Exosomes and their role in the micro-/macro-environment: a comprehensive review. J Biomed Res 31:386-394|
|Blackburn, Patrick R; Tischer, Alexander; Zimmermann, Michael T et al. (2017) A Novel Kleefstra Syndrome-associated Variant That Affects the Conserved TPLX Motif within the Ankyrin Repeat of EHMT1 Leads to Abnormal Protein Folding. J Biol Chem 292:3866-3876|
|Walz, Amy; Ugolkov, Andrey; Chandra, Sunandana et al. (2017) Molecular Pathways: Revisiting Glycogen Synthase Kinase-3? as a Target for the Treatment of Cancer. Clin Cancer Res 23:1891-1897|
|Yellow, Winta; Bamlet, William R; Oberg, Ann L et al. (2017) Association between Alcohol Consumption, Folate Intake, and Risk of Pancreatic Cancer: A Case-Control Study. Nutrients 9:|
|Luo, Kuntian; Li, Yunhui; Yin, Yujiao et al. (2017) USP49 negatively regulates tumorigenesis and chemoresistance through FKBP51-AKT signaling. EMBO J 36:1434-1446|
|Liou, Geou-Yarh; Bastea, Ligia; Fleming, Alicia et al. (2017) The Presence of Interleukin-13 at Pancreatic ADM/PanIN Lesions Alters Macrophage Populations and Mediates Pancreatic Tumorigenesis. Cell Rep 19:1322-1333|
|Cho, Dong Seong; Doles, Jason D (2017) Single cell transcriptome analysis of muscle satellite cells reveals widespread transcriptional heterogeneity. Gene 636:54-63|
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