This proposal investigates the molecular basis of information flow in cancer cells. The proposed Northwestern University Physical Sciences-Oncology (NU-PSOC) program is organized along a hierarchy of structure and function and consists of five projects areas, each focused on different aspects of the storage and expression of genetic information. Each project integrates methods and ideas of experimental molecular and cell biology with experimental methods and theoretical ideas from the physical sciences to achieve a quantitative and predictive understanding of fundamental mechanisms and principles in the regulation and expression of genes, in normal health and development, and in cancer.

Public Health Relevance

is through its goal of generating new understanding of fundamental mechanisms in cancer molecular biology, which should lead to better diagnostics and therapeutics. This proposal investigates the molecular basis of information flow in cancer cells. The proposed Northwestern University Physical Sciences-Oncology (NU-PSOC) program is organized along a hierarchy of structure and function and consists of five projects areas, each focused on different aspects of the storage and expression of genetic information. Each project integrates methods and ideas of experimental molecular and cell biology with experimental methods and theoretical ideas from the physical sciences to achieve a quantitative and predictive understanding of fundamental mechanisms and principles in the regulation and expression of genes, in normal health and development, and in cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center--Cooperative Agreements (U54)
Project #
3U54CA143869-05S1
Application #
8707085
Study Section
Special Emphasis Panel (ZCA1-SRLB-9 (O1))
Program Officer
Ogunbiyi, Peter
Project Start
2009-09-28
Project End
2014-07-31
Budget Start
2013-08-01
Budget End
2014-07-31
Support Year
5
Fiscal Year
2013
Total Cost
$35,688
Indirect Cost
$12,589
Name
Northwestern University at Chicago
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
005436803
City
Chicago
State
IL
Country
United States
Zip Code
60611
Serebryannyy, Leonid A; Yemelyanov, Alex; Gottardi, Cara J et al. (2017) Nuclear ?-catenin mediates the DNA damage response via ?-catenin and nuclear actin. J Cell Sci 130:1717-1729
Voong, Lilien N; Xi, Liqun; Sebeson, Amy C et al. (2016) Insights into Nucleosome Organization in Mouse Embryonic Stem Cells through Chemical Mapping. Cell 167:1555-1570.e15
Serebryannyy, Leonid A; Cruz, Christina M; de Lanerolle, Primal (2016) A Role for Nuclear Actin in HDAC 1 and 2 Regulation. Sci Rep 6:28460
Hill, Steven M; Heiser, Laura M; Cokelaer, Thomas et al. (2016) Inferring causal molecular networks: empirical assessment through a community-based effort. Nat Methods 13:310-8
Zhao, Baobing; Mei, Yang; Schipma, Matthew J et al. (2016) Nuclear Condensation during Mouse Erythropoiesis Requires Caspase-3-Mediated Nuclear Opening. Dev Cell 36:498-510
Serebryannyy, Leonid A; Parilla, Megan; Annibale, Paolo et al. (2016) Persistent nuclear actin filaments inhibit transcription by RNA polymerase II. J Cell Sci 129:3412-25
Chuang, Yishan; Hung, Michelle E; Cangelose, Brianne K et al. (2016) Regulation of the IL-10-driven macrophage phenotype under incoherent stimuli. Innate Immun 22:647-657
Shah, M Y; Martinez-Garcia, E; Phillip, J M et al. (2016) MMSET/WHSC1 enhances DNA damage repair leading to an increase in resistance to chemotherapeutic agents. Oncogene 35:5905-5915
Yildirim, Ilyas; Chakraborty, Debayan; Disney, Matthew D et al. (2015) Computational investigation of RNA CUG repeats responsible for myotonic dystrophy 1. J Chem Theory Comput 11:4943-58
Khalkhali-Ellis, Zhila; Kirschmann, Dawn A; Seftor, Elisabeth A et al. (2015) Divergence(s) in nodal signaling between aggressive melanoma and embryonic stem cells. Int J Cancer 136:E242-51

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