The Washington University Pancreatic Cancer Specialized Program of Research Excellence (SPORE) is a highly translational cancer research program focused entirely on the deadliest form of the disease, pancreatic ductal adenocarcinoma (PDAC). Our outstanding investigators have complementary expertise in basic and clinical sciences, and our teams leverage individual expertise in immunology, drug development, genomics, and imaging to develop novel diagnostic and therapeutic approaches to PDAC. This SPORE includes four research projects, an administrative core, two shared-resources cores, and developmental research and career enhancement programs. With the help of our External and Internal Advisory Boards, we have intentionally selected the projects that have the greatest potential to impact PDAC. All four of our selected projects include a therapeutic trial, and two take advantage of immunologic discoveries made at WU. We have two projects that utilize small molecule inhibitors of pathways that are known to be active in PDAC. The four projects in our application are designed to have significant potential to change clinical practice within five years. Project 1: Overcoming Tumor-Induced Immune Suppression to Improve Responses to Immunotherapy Project 2: Clinical Development of the Pancreatic Cancer Drug Conjugate SW V-49 Project 3: Combination Inhibition of ERK for Pancreatic Cancer Treatment Project 4: Translation and Preclinical Studies of a Personalized Pancreatic Cancer Vaccine Our long-term goal is to improve survival of patients diagnosed with PDAC. To achieve this, we will promote institutional and inter-institutional collaborative science, with an emphasis on translation. We expect that no singular approach will solve PDAC, and fully commit to supporting the development of novel ideas and young investigators. Our SPORE will provide access to pancreatic cancer-specific resources to facilitate this mission.
The goal of the proposed research is to improve our understanding of pancreatic cancer biology. Specifically, we will develop new approaches to detect and treat pancreatic cancers in order to reduce morbidity and mortality.
|Pati, Maria Laura; Niso, Mauro; Spitzer, Dirk et al. (2018) Multifunctional thiosemicarbazones and deconstructed analogues as a strategy to study the involvement of metal chelation, Sigma-2 (?2) receptor and P-gp protein in the cytotoxic action: In vitro and in vivo activity in pancreatic tumors. Eur J Med Chem 144:359-371|
|Brauer, David G; Ohman, Kerri A; Jaques, David P et al. (2018) Surgeon Variation in Intraoperative Supply Cost for Pancreaticoduodenectomy: Is Intraoperative Supply Cost Associated with Outcomes? J Am Coll Surg 226:37-45.e1|
|Mirlekar, Bhalchandra; Michaud, Daniel; Searcy, Ryan et al. (2018) IL35 Hinders Endogenous Antitumor T-cell Immunity and Responsiveness to Immunotherapy in Pancreatic Cancer. Cancer Immunol Res 6:1014-1024|
|Nywening, Timothy M; Belt, Brian A; Cullinan, Darren R et al. (2018) Targeting both tumour-associated CXCR2+ neutrophils and CCR2+ macrophages disrupts myeloid recruitment and improves chemotherapeutic responses in pancreatic ductal adenocarcinoma. Gut 67:1112-1123|
|Brenot, Audrey; Knolhoff, Brett L; DeNardo, David G et al. (2018) SNAIL1 action in tumor cells influences macrophage polarization and metastasis in breast cancer through altered GM-CSF secretion. Oncogenesis 7:32|
|Meyer, Melissa A; Baer, John M; Knolhoff, Brett L et al. (2018) Breast and pancreatic cancer interrupt IRF8-dependent dendritic cell development to overcome immune surveillance. Nat Commun 9:1250|
|Meyer, Melissa A; DeNardo, David G (2018) Better Together: B7S1 Checkpoint Blockade Synergizes with anti-PD1. Immunity 48:621-623|
|Jiang, Hongmei; Xu, Mai; Li, Lin et al. (2018) Concurrent HER or PI3K Inhibition Potentiates the Antitumor Effect of the ERK Inhibitor Ulixertinib in Preclinical Pancreatic Cancer Models. Mol Cancer Ther 17:2144-2155|
|Waters, Andrew M; Der, Channing J (2018) KRAS: The Critical Driver and Therapeutic Target for Pancreatic Cancer. Cold Spring Harb Perspect Med 8:|
|Zhang, Daoxiang; Li, Lin; Jiang, Hongmei et al. (2018) Tumor-Stroma IL1?-IRAK4 Feedforward Circuitry Drives Tumor Fibrosis, Chemoresistance, and Poor Prognosis in Pancreatic Cancer. Cancer Res 78:1700-1712|
Showing the most recent 10 out of 25 publications