The Biostatistics Core provides state-of-the-art statistical support for all SARC SPORE projects and investigators. The overall goal ofthe SARC SPORE is to better understand the etiology of sarcoma and its histologies, and to develop biomarkers and M new treatment options for sarcoma patients. The Biostatistics Core will provide statistical consultation and collaboration on all aspects of design, analysis and interpretation of the clinical trials and laboratory experiments. Core personnel will work closely with project leaders to ensure that the Biostatistics Core provides state-of-the-art statistical support. The primary objectives of the Biostatistics Core are to: 1. Provide study design and review all laboratory, animal, and clinical studies including feasibility assessment, power analysis, and sample size estimation; 2. Collaborate in the project data analysis, interpretation of results, and writing of final study reports and manuscripts; 3. Facilitate prospective collection, entry and quality control of data for the basic science experiments; and collaborate with the clinical trials core to facilitate quality control of clinical data;and 4. Develop and evaluate statistical methods for experimental design and data analysis. To ensure those aims are met, constant, regular communication among core personnel of this Biostatistics Core, SPORE projects and other Cores is needed, Regular weeKly conference calis among project and core leaders will review progress on clinical trials, laboratory studies and data analysis, ensure issues are recognized/addressed, and apprise leaders of developments.
The SARC Sarcoma SPORE Biostatistics Core (Core D) is a cross-cutting SPORE resource, which will perform crucial roles in planning, conducting and analyzing translational and clinical sarcoma research in the main projects, other cores (e.g. Clinical Trials Core - Core C), developmental projects, and career development award efforts. Therefore, the Biostatistics Core is relevant, and essential, to achieving the SPORE goals.
|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|
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