instructiors): The broad objective of the Administrative Core is to provide multiple levels of program management support to the project and core investigators. Dr. Segal, as program director, will be responsible for all aspects of program management. To facilitate communication, coordination and planning among the projects and the INP Core, Dr. Segal will be assisted by a scientific program coordinator. Dr. Segal will also be aided by the Cancer Biology Business Office to assist her in the fiscal management of the award. The Administrative Core has three specific aims:
Aim one is to provide effective communication, coordination and planning for the program. Dr. Segal and the scientific program coordinator will schedule and facilitate monthly research -in- progress meetings for project and core investigators. The internal advisory board will be invited to this meeting on a semi-annual basis, and the external advisor will be invited to attend yearly, to provide their fresh perspectives and guidance. Following these advisory meetings, Dr. Segal and the program coordinator will synthesize the evaluations and recommendations from the advisory board and distribute them to all project and core investigators.
Aim two is to assist the Dr. Segal with fiscal management of the award. This includes processing award notices from the NIH, managing project budgets, and assisting in the preparation of annual progress reports to the NIH. Our Business Office is staffed with grants management specialists who concentrate on either pre-award or post-award aspects of research awards.
Aim three is to provide clerical support to Dr. Segal for tracking annual renewals of animal and human protocols, manuscript preparation, traveling and scheduling as it pertains to the program.
|Pak, Ekaterina; Segal, Rosalind A (2016) Hedgehog Signal Transduction: Key Players, Oncogenic Drivers, and Cancer Therapy. Dev Cell 38:333-44|
|Bandopadhayay, Pratiti; Ramkissoon, Lori A; Jain, Payal et al. (2016) MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism. Nat Genet 48:273-82|
|Yuzugullu, Haluk; Von, Thanh; Thorpe, Lauren M et al. (2016) NTRK2 activation cooperates with PTEN deficiency in T-ALL through activation of both the PI3K-AKT and JAK-STAT3 pathways. Cell Discov 2:16030|
|Stevens, Mark M; Maire, Cecile L; Chou, Nigel et al. (2016) Drug sensitivity of single cancer cells is predicted by changes in mass accumulation rate. Nat Biotechnol 34:1161-1167|
|Verreault, Maite; Schmitt, Charlotte; Goldwirt, Lauriane et al. (2016) Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas. Clin Cancer Res 22:1185-96|
|Ni, Jing; Ramkissoon, Shakti H; Xie, Shaozhen et al. (2016) Combination inhibition of PI3K and mTORC1 yields durable remissions in mice bearing orthotopic patient-derived xenografts of HER2-positive breast cancer brain metastases. Nat Med 22:723-6|
|Filbin, Mariella G; Segal, Rosalind A (2015) How neuronal activity regulates glioma cell proliferation. Neuro Oncol 17:1543-4|
|Brastianos, Priscilla K; Carter, Scott L; Santagata, Sandro et al. (2015) Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets. Cancer Discov 5:1164-77|
|Zhou, Pengcheng; Erfani, Sonia; Liu, Zeyi et al. (2015) CD151-Î±3Î²1 integrin complexes are prognostic markers of glioblastoma and cooperate with EGFR to drive tumor cell motility and invasion. Oncotarget 6:29675-93|
|Zhao, Xuesong; Ponomaryov, Tatyana; Ornell, Kimberly J et al. (2015) RAS/MAPK Activation Drives Resistance to Smo Inhibition, Metastasis, and Tumor Evolution in Shh Pathway-Dependent Tumors. Cancer Res 75:3623-35|
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