? ADMINISTRATIVE CORE Cornell University will be the lead institution of our Center on the Physics of Cancer Metabolism that constitutes a multi-institutional effort involving 20 key personnel from Cornell University Ithaca, Weill Cornell Medicine (WCM), Memorial Sloan Kettering Cancer Center (MSKCC), University of Texas MD Anderson Cancer Center, University of California ? San Francisco, and Purdue University. The Administrative Core team will be responsible for organizing and providing resources for effective management and oversight of these individual sites. Given our focus on collaboration, we will use a Multiple PI Leadership approach drawing on the physical sciences and cancer biology expertise of both PIs as well as their respective home institutions. Guidance to the PIs will be provided through the Center Advisory Committee. Furthermore, a Center Administrator will manage day-to-day activities, including subcontracts with our partner institutions and all scientific, administrative, budgetary, and operational aspects of the Center. The overall goal of the Administrative Core will be to guarantee effective administrative and organizational capabilities both within our Center and with the broader Physical Sciences Oncology Network (PSON). This goal will be accomplished through 3 specific aims.
Aim 1 : To manage and effectively deploy the Center's resources to advance transdisciplinary physical sciences research, training, and outreach.
Aim 2 : To enhance the exchange of information and ideas among all Center researchers as well as with the PSON.
Aim 3 : To establish Committees for Center guidance and institute appropriate infrastructure and processes for transparent, effective, and iterative evaluation of all Center activities. The Administrative Core will synergize with all components of the Center to ensure successful integration of Projects and Cores, the Education and Outreach Unit, and research performed through Pilot and Transnetwork Projects.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center--Cooperative Agreements (U54)
Project #
5U54CA210184-04
Application #
9748458
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2019-08-01
Budget End
2020-07-31
Support Year
4
Fiscal Year
2019
Total Cost
Indirect Cost
Name
Cornell University
Department
Type
DUNS #
872612445
City
Ithaca
State
NY
Country
United States
Zip Code
14850
Bakhoum, Samuel F; Ngo, Bryan; Laughney, Ashley M et al. (2018) Chromosomal instability drives metastasis through a cytosolic DNA response. Nature 553:467-472
Singh, Ankur; Brito, Ilana; Lammerding, Jan (2018) Beyond Tissue Stiffness and Bioadhesivity: Advanced Biomaterials to Model Tumor Microenvironments and Drug Resistance. Trends Cancer 4:281-291
Ramakrishnan, N; Sreeja, K K; Roychoudhury, Arpita et al. (2018) Excess area dependent scaling behavior of nano-sized membrane tethers. Phys Biol 15:026002
Gritsenko, Pavlo G; Friedl, Peter (2018) Adaptive adhesion systems mediate glioma cell invasion in complex environments. J Cell Sci 131:
Lundquist, Mark R; Goncalves, Marcus D; Loughran, Ryan M et al. (2018) Phosphatidylinositol-5-Phosphate 4-Kinases Regulate Cellular Lipid Metabolism By Facilitating Autophagy. Mol Cell 70:531-544.e9
Goncalves, Marcus D; Hwang, Seo-Kyoung; Pauli, Chantal et al. (2018) Fenofibrate prevents skeletal muscle loss in mice with lung cancer. Proc Natl Acad Sci U S A 115:E743-E752
Iyengar, Neil M; Chen, I-Chun; Zhou, Xi K et al. (2018) Adiposity, Inflammation, and Breast Cancer Pathogenesis in Asian Women. Cancer Prev Res (Phila) 11:227-236
Zahid, H; Subbaramaiah, K; Iyengar, N M et al. (2018) Leptin regulation of the p53-HIF1?/PKM2-aromatase axis in breast adipose stromal cells: a novel mechanism for the obesity-breast cancer link. Int J Obes (Lond) 42:711-720
Hopkins, Benjamin D; Pauli, Chantal; Du, Xing et al. (2018) Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature 560:499-503
Croessmann, Sarah; Sheehan, Jonathan H; Lee, Kyung-Min et al. (2018) PIK3CA C2 Domain Deletions Hyperactivate Phosphoinositide 3-kinase (PI3K), Generate Oncogene Dependence, and Are Exquisitely Sensitive to PI3K? Inhibitors. Clin Cancer Res 24:1426-1435

Showing the most recent 10 out of 46 publications