CORE A (Administration and Informatics) The Administrative Core is responsible for program planning and evaluation, operations management, organization of meetings, financial stewardship, and informatics services. Key Core A functions are to: ?Provide scientific and administrative oversight to all components of the Consortium. ?Coordinate communication and organize meetings between CRC investigators, staff, DSMB, external and internal advisory boards, ?Execute effective planning and evaluation systems to monitor program performance and efficiency in regards to resource management. ?Monitor for compliance with NIH, NCI, FDA, DHHS, and participating organizations, and render reports concerning such monitoring. Monitor use of human subjects, animal subjects, and tissue specimens. ?Develop and maintain specific policies and procedures to ensure the quality and confidentiality of all CRC data and associated information management systems. Maintain ongoing research into the enhancement of said policies to ensure compliance with evolving regulatory and legislative requirements. ?Manage grants/contracts, perform fiscal oversight /management, and disburse funds. ?Provide information management systems, including clinical, basic science, and administrate data collection, storage, and analysis instruments. ?Expand current information management systems to incorporate new data sets and data management requirements. ?Provide the community and CLL patients specifically, with information regarding CRC research activities and general OIL educational materials.
The primary objective of Core A is to enable the efficient and effective operation and coordination of consortium-wide projects and cores. This objective is motivated by the CRCs overall mission to help develop curative strategies for patients with Chronic Lymphocytic Leukemia.
|Mani, R; Mao, Y; Frissora, F W et al. (2015) Tumor antigen ROR1 targeted drug delivery mediated selective leukemic but not normal B-cell cytotoxicity in chronic lymphocytic leukemia. Leukemia 29:346-55|
|Veronese, A; Pepe, F; Chiacchia, J et al. (2015) Allele-specific loss and transcription of the miR-15a/16-1 cluster in chronic lymphocytic leukemia. Leukemia 29:86-95|
|Woyach, Jennifer A; Furman, Richard R; Liu, Ta-Ming et al. (2014) Resistance mechanisms for the Bruton's tyrosine kinase inhibitor ibrutinib. N Engl J Med 370:2286-94|
|Chen, Wenbing; Han, Yanyan; Peng, Xiaohua (2014) Aromatic nitrogen mustard-based prodrugs: activity, selectivity, and the mechanism of DNA cross-linking. Chemistry 20:7410-8|
|Stephens, D M; Ruppert, A S; Jones, J A et al. (2014) Impact of targeted therapy on outcome of chronic lymphocytic leukemia patients with relapsed del(17p13.1) karyotype at a single center. Leukemia 28:1365-8|
|Cheney, Carolyn M; Stephens, Deborah M; Mo, Xiaokui et al. (2014) Ocaratuzumab, an Fc-engineered antibody demonstrates enhanced antibody-dependent cell-mediated cytotoxicity in chronic lymphocytic leukemia. MAbs 6:749-55|
|Strati, Paolo; Ferrajoli, Alessandra; Lerner, Susan et al. (2014) Fludarabine, cyclophosphamide and rituximab plus granulocyte macrophage colony-stimulating factor as frontline treatment for patients with chronic lymphocytic leukemia. Leuk Lymphoma 55:828-33|
|Cui, Bing; Chen, Liguang; Zhang, Suping et al. (2014) MicroRNA-155 influences B-cell receptor signaling and associates with aggressive disease in chronic lymphocytic leukemia. Blood 124:546-54|
|Riches, John C; Gribben, John G (2014) Hanging tough: CMV-specific CD8+ T cells in CLL. Blood 123:608-9|
|Fecteau, Jessie-F; Corral, Laura G; Ghia, Emanuela M et al. (2014) Lenalidomide inhibits the proliferation of CLL cells via a cereblon/p21(WAF1/Cip1)-dependent mechanism independent of functional p53. Blood 124:1637-44|
Showing the most recent 10 out of 227 publications