The Integrated Translational Science Center (ITSC) formed between SWOG, Cold Spring Harbor Laboratory (CSHL), and The Jackson Laboratory (JAX) provides a powerful combination of clinical and basic research expertise for application to cancer medicine. CSHL and JAX are both NCI-designated Cancer Centers and represent a significant collective experience in cancer gene discovery, the functional genomics of cancer, innovative tumor modeling, and the development of novel technologies to interrogate the disease. SWOG is a premier clinical trials organization that has established the standard of care for multiple cancer types over the past several decades. This alliance will bridge the gap between the laboratory and the clinic by elucidating the key clinical problems and challenges in oncology that can be addressed in the laboratory, discovering new diagnostic and therapeutic approaches that can be integrated into clinical trials, and providing a conduit for clinical trial results to be re-interpreted in the laboratory. This relationship will lead to a clearer understanding of the mechanisms underlying cancer and advance translational research aimed at developing effective targeted therapies. Both CSHL and JAX have used their extensive knowledge of the molecular alterations in human cancer to generate a diverse array of genetically modified or primary human- derived (PDX) xenograft mouse models of human cancer, and these models will be collectively utilized to identify new therapeutic vulnerabilities, determine mechanisms of primary or secondary drug resistance, and develop novel diagnostic strategies. Such information will be used to generate new hypotheses in regard to potential predictive biomarkers that can be studied in randomized clinical trials being conducted by SWOG. Specific examples of novel expertise include single cell sequencing, circulating DNA analysis, co-clinical trials in animal models, computational prediction of resistance from genomic data, and in silico and animal modeling of therapeutic combinations to optimize initial potency and avoid resistance. The scientific endeavors of CSHL and JAX will therefore inform ongoing clinical trials and establish a mechanism for fostering translational cancer research.
This CSHL-JAX-SWOG ITSC will inform ongoing clinical trials and facilitate collaboration between research scientists and SWOG member oncologists. SWOG and other NTCN centers will benefit from new research findings and approaches that provide critical information on the molecular basis of cancer development and growth, and resistance to therapy. This alliance promises to improve the diagnosis and treatment of cancer.
|Chio, Iok In Christine; Tuveson, David A (2017) ROS in Cancer: The Burning Question. Trends Mol Med 23:411-429|
|Öhlund, Daniel; Handly-Santana, Abram; Biffi, Giulia et al. (2017) Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer. J Exp Med 214:579-596|
|Roe, Jae-Seok; Hwang, Chang-Il; Somerville, Tim D D et al. (2017) Enhancer Reprogramming Promotes Pancreatic Cancer Metastasis. Cell 170:875-888.e20|
|Feigin, Michael E; Garvin, Tyler; Bailey, Peter et al. (2017) Recurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma. Nat Genet 49:825-833|
|Othus, M; Wood, B L; Stirewalt, D L et al. (2016) Effect of measurable ('minimal') residual disease (MRD) information on prediction of relapse and survival in adult acute myeloid leukemia. Leukemia 30:2080-2083|
|Park, Juwon; Wysocki, Robert W; Amoozgar, Zohreh et al. (2016) Cancer cells induce metastasis-supporting neutrophil extracellular DNA traps. Sci Transl Med 8:361ra138|
|Baker, Lindsey A; Tiriac, Hervé; Clevers, Hans et al. (2016) Modeling pancreatic cancer with organoids. Trends Cancer 2:176-190|
|Chio, Iok In Christine; Jafarnejad, Seyed Mehdi; Ponz-Sarvise, Mariano et al. (2016) NRF2 Promotes Tumor Maintenance by Modulating mRNA Translation in Pancreatic Cancer. Cell 166:963-976|
|Biffi, G; Öhlund, D; Tuveson, D (2016) Building up the tension between the epithelial and stromal compartment in pancreatic ductal adenocarcinoma. Cell Death Differ 23:1265-6|
|Hwang, Chang-Il; Boj, Sylvia F; Clevers, Hans et al. (2016) Preclinical models of pancreatic ductal adenocarcinoma. J Pathol 238:197-204|
Showing the most recent 10 out of 14 publications