The Cell Signaling Program provides a broad base of research into mechanisms of cell and molecular biology to facilitate discovery and validation of novel targets for cancer translational and clinical research. Targets involved in various fundamental processes may be utilized for cancer detection, diagnosis, prevention, and therapy as well as for monitoring efficacy of therapeutic interventions. Cell signaling encompasses multiple biochemical circuits in cells, including those involved in regulation of growth (size and synthesis), proliferation (duplication and division), stress responses and survival vs. apoptosis. The overall goals of this Program are to support outstanding research and emphasize the importance of understanding perturbations of signaling in cancer cells. Cell signaling proteins, especially receptors and protein kinases, are validated targets for development of therapies by pharmaceutical and biotechnology companies worldwide. The Cell Signaling Program is a resource for research on cancer composed of 31 members from 11 different departments within the University of Virginia, including 15 new members since the last renewal. It comprises a unique mix of faculty not replicated in any other activity at the University, drawing people from different departments in different schools within the University, and from various research Centers, who otherwise are isolated by administrative and organizational boundaries. We collaborate effectively with other Cancer Center Programs, providing expertise and knowledge to a variety of cancer-related projects. Over 25% of our 500 publications have been co-authored with members of other Programs and 10% were coauthored with members of this Program. This is a cancer-oriented group with $4.2M in NCI support, and $6.5M in other NIH grants and $11.6M in total peer-reviewed support. Research can be clustered into three thematic areas: 1) signal initiation by various types of cell-surface receptors, 2) signal transduction by GTP proteins and protein kinases and phosphatases and 3) chemical biology of small molecules that target specific proteins. This Program intends to tap our institutional strength in cell signaling research to close the circle of bedside-bench-bedside with discovery of novel targets, testing of small molecule inhibitors of those targets, and molecular assessments of therapies.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA044579-19
Application #
7771652
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2009-02-01
Budget End
2010-01-31
Support Year
19
Fiscal Year
2009
Total Cost
$30,692
Indirect Cost
Name
University of Virginia
Department
Type
DUNS #
065391526
City
Charlottesville
State
VA
Country
United States
Zip Code
22904
Knapp, Kiley A; Pires, Eusebio S; Adair, Sara J et al. (2018) Evaluation of SAS1B as a target for antibody-drug conjugate therapy in the treatment of pancreatic cancer. Oncotarget 9:8972-8984
Kedzierska, Katarzyna Z; Gerber, Livia; Cagnazzi, Daniele et al. (2018) SONiCS: PCR stutter noise correction in genome-scale microsatellites. Bioinformatics 34:4115-4117
Zhang, Xuewei; Kitatani, Kazuyuki; Toyoshima, Masafumi et al. (2018) Ceramide Nanoliposomes as a MLKL-Dependent, Necroptosis-Inducing, Chemotherapeutic Reagent in Ovarian Cancer. Mol Cancer Ther 17:50-59
Cruickshanks, Nichola; Zhang, Ying; Hine, Sarah et al. (2018) Discovery and Therapeutic Exploitation of Mechanisms of Resistance to MET Inhibitors in Glioblastoma. Clin Cancer Res :
Balogh, Kristen N; Templeton, Dennis J; Cross, Janet V (2018) Macrophage Migration Inhibitory Factor protects cancer cells from immunogenic cell death and impairs anti-tumor immune responses. PLoS One 13:e0197702
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Rodriguez, Anthony B; Peske, J David; Engelhard, Victor H (2018) Identification and Characterization of Tertiary Lymphoid Structures in Murine Melanoma. Methods Mol Biol 1845:241-257
Stowman, Anne M; Hickman, Alexandra W; Mauldin, Ileana S et al. (2018) Lymphoid aggregates in desmoplastic melanoma have features of tertiary lymphoid structures. Melanoma Res 28:237-245
Melhuish, Tiffany A; Kowalczyk, Izabela; Manukyan, Arkadi et al. (2018) Myt1 and Myt1l transcription factors limit proliferation in GBM cells by repressing YAP1 expression. Biochim Biophys Acta Gene Regul Mech 1861:983-995
Kulling, Paige M; Olson, Kristine C; Olson, Thomas L et al. (2018) Calcitriol-mediated reduction in IFN-? output in T cell large granular lymphocytic leukemia requires vitamin D receptor upregulation. J Steroid Biochem Mol Biol 177:140-148

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