The Administration Core (Core A) will coordinate and support the programmatic, fiscal, oversight and developmental endeavors upon which the translational success of the SARC Sarcoma SPORE depends. The goals of the SPORE are to translate biological and technological advances into improvements in prevention, diagnostics, predictors of outcome, and particularly -advances in the treatment of sarcoma. The SARC Sarcoma SPORE is anchored by multiple researchers from SARC, Harvard, and MD Anderson Cancer Center, but also includes key individual researchers from Stanford University, Columbia University and The University of Michigan. The researchers represent medical and pediatric oncology and the projects explore both soft tissue and bone sarcomas. Four major projects are proposed: 1) Rational HDACi-based therapeutic strategies for the treatment of genetically complex STS;2) Developing effective combination therapies for malignant peripheral nerve sheath tumor (MPNST);3) Identification of biomarkers of response to G-protein coupled receptors and novei therapeutic targets in Ewing's sarcoma;and 4) Developing quantitative imaging biomarkers for assessing therapeutic response to sarcoma therapy. These projects are integrated and supported by 4 cores: 1) Administration, Evaluation and Planning;2) Tissue and Pathology; 3) Clinical Trials;and 4) Biostatistics. The SP0RE application outlines a Developmental Research Program that includes a plan for selection of new projects as well as 14 proposed developmental pilot projects. We also inciude a Career Development Program that outlines a mechanism for the identification and support of talented young investigators in translational or clinical sarcoma research. The projects and cores proposed in this application are highly integrated and are poised to take maximum advantage ofthe SPORE mechanism to achieve translational goals. This SPORE joins the foremost sarcoma investigators and state-of-the art research projects with the multi-institution, collaborative strength of SARC and commitments from leading institutions to produce successful translational advances in the diagnosis, treatment, and prevention of sarcoma.
The SPORE progrann will advance sarcoma therapeutics by combining and integrating nation-wide translational research strengths. Success in this endeavor will require capable and well-supported administrative center, which will maximize opportunities for existing projects and cores, coordinate oversight ofthe SPORE, and encourage career development and development of promising new project concepts.
|Feng, Yong; Sassi, Slim; Shen, Jacson K et al. (2015) Targeting CDK11 in osteosarcoma cells using the CRISPR-Cas9 system. J Orthop Res 33:199-207|
|Monument, Michael J; Johnson, Kirsten M; McIlvaine, Elizabeth et al. (2014) Clinical and biochemical function of polymorphic NR0B1 GGAA-microsatellites in Ewing sarcoma: a report from the Children's Oncology Group. PLoS One 9:e104378|
|Choy, Edwin; Butrynski, James E; Harmon, David C et al. (2014) Phase II study of olaparib in patients with refractory Ewing sarcoma following failure of standard chemotherapy. BMC Cancer 14:813|
|Kernstine, Kemp H; Moon, James; Kraut, Michael J et al. (2014) Trimodality therapy for superior sulcus non-small cell lung cancer: Southwest Oncology Group-Intergroup Trial S0220. Ann Thorac Surg 98:402-10|
|Sankar, Savita; Theisen, Emily R; Bearss, Jared et al. (2014) Reversible LSD1 inhibition interferes with global EWS/ETS transcriptional activity and impedes Ewing sarcoma tumor growth. Clin Cancer Res 20:4584-97|
|Zhang, Pingyu; Garnett, Jeannine; Creighton, Chad J et al. (2014) EZH2-miR-30d-KPNB1 pathway regulates malignant peripheral nerve sheath tumour cell survival and tumourigenesis. J Pathol 232:308-18|
|Sioletic, Stefano; Czaplinski, Jeffrey; Hu, Lan et al. (2014) c-Jun promotes cell migration and drives expression of the motility factor ENPP2 in soft tissue sarcomas. J Pathol 234:190-202|
|Chen, Eleanor Y; DeRan, Michael T; Ignatius, Myron S et al. (2014) Glycogen synthase kinase 3 inhibitors induce the canonical WNT/?-catenin pathway to suppress growth and self-renewal in embryonal rhabdomyosarcoma. Proc Natl Acad Sci U S A 111:5349-54|
|Krook, Melanie A; Nicholls, Lauren A; Scannell, Christopher A et al. (2014) Stress-induced CXCR4 promotes migration and invasion of ewing sarcoma. Mol Cancer Res 12:953-64|
|Jia, Bin; Choy, Edwin; Cote, Gregory et al. (2014) Cyclin-dependent kinase 11 (CDK11) is crucial in the growth of liposarcoma cells. Cancer Lett 342:104-12|
Showing the most recent 10 out of 13 publications