The UC Davis Cancer Center, an integrated program with Lawrence Livermore National Labs (LLNL), is a matrix organization under the aegis of the UC Davis Health System (combining the UC Davis School of Medicine and the UC Davis Medical Center), and the University of California, Davis. Located on the campus of the UC Davis Medical Center in Sacramento, California, the cancer center's administrative, clinical and research facilities are under the leadership of the Principal Investigator of this P30 competitive renewal;an initial P30 was awarded to the Cancer Center on July 1, 2002. The Cancer Center draws its 186 members from the faculty of UC Davis and investigators at the LLNL, the USDA Western Human Nutrition Research Center and the California Department of Public Health. Peer-reviewed funding for UC Davis Cancer Center members totals $81,918,736.00 of which $21,771,164.00 (direct costs) is provided by the NCI. Investigators at the other organizations contributing membership are also provided research funding through the US Department of Energy, the US Department of Agriculture, and the State of California respectively. At the UC Davis Cancer Center, research is organized into six programs: (1) Molecular Oncology, (2) Comparative Oncology, (3) Cancer Therapeutics, (4) Population Sciences and Health Disparities, (5) Prostate Cancer, (6) Biomedical Technology. This competitive renewal for the P30 [Cancer Center Support Grant] proposes support for (1) senior leadership, (2) program leadership, (3) developmental programs, (4) administration, (5) planning and evaluation activities, (6) nine shared resources including genomics, optical biology, mouse biology, the clinical trials support unit, biostatistics, clinical and molecular pharmacology, animal imaging, biospecimen repository and combinatorial chemistry, (7) the Protocol Review and Monitoring System, (8) protocol-specific research, and (9) Data Safety and Monitoring.
The proposed Cancer Center Support Grant provides the infrastructure for the cancer research enterprise at UC Davis and for center members at other institutions. This infrastructure promotes collaboration and and scientific excellence in cancer research and the application of research to the care of patients benefiting from research at UC Davis and through dissemination, patients everywhere.
|Zhang, Jin; Lucchesi, Christopher; Chen, Xinbin (2016) A new function for p53 tetramerization domain in cell fate control. Cell Cycle 15:2854-2855|
|Vinall, Ruth L; Tepper, Clifford G; Ripoll, Alexandra A Z et al. (2016) Decreased expression of let-7c is associated with non-response of muscle-invasive bladder cancer patients to neoadjuvant chemotherapy. Genes Cancer 7:86-97|
|Kirschbaum, Mark H; Frankel, Paul; Synold, Timothy W et al. (2016) A phase I pharmacodynamic study of GTI-2040, an antisense oligonucleotide against ribonuclotide reductase, in acute leukemias: a California Cancer Consortium study. Leuk Lymphoma 57:2307-14|
|TachÃ©, VÃ©ronique; Bivina, Liga; White, Sophie et al. (2016) Lipoyltransferase 1 Gene Defect Resulting in Fatal Lactic Acidosis in Two Siblings. Case Rep Obstet Gynecol 2016:6520148|
|Lara, Joshua; Brunson, Ann; Keegan, Theresa H M et al. (2016) Determinants of Survival for Adolescents and Young Adults with Urothelial Bladder Cancer: Results from the California Cancer Registry. J Urol 196:1378-1382|
|Faisal, Farzana A; Sundi, Debasish; Tosoian, Jeffrey J et al. (2016) Racial Variations in Prostate Cancer Molecular Subtypes and Androgen Receptor Signaling Reflect Anatomic Tumor Location. Eur Urol 70:14-7|
|Dang, Julie H T; Chen Jr, Moon S (2016) Increasing Hepatitis B Testing and Linkage to Care of Foreign-Born Asians, Sacramento, California, 2012-2013. Public Health Rep 131 Suppl 2:119-24|
|Rowson-Hodel, Ashley R; Berg, Anastasia L; Wald, Jessica H et al. (2016) Hexamethylene amiloride engages a novel reactive oxygen species- and lysosome-dependent programmed necrotic mechanism to selectively target breast cancer cells. Cancer Lett 375:62-72|
|Zhao, Yong; Tu, Mei-Juan; Wang, Wei-Peng et al. (2016) Genetically engineered pre-microRNA-34a prodrug suppresses orthotopic osteosarcoma xenograft tumor growth via the induction of apoptosis and cell cycle arrest. Sci Rep 6:26611|
|Monjazeb, Arta M; Kent, Michael S; Grossenbacher, Steven K et al. (2016) Blocking Indolamine-2,3-Dioxygenase Rebound Immune Suppression Boosts Antitumor Effects of Radio-Immunotherapy in Murine Models and Spontaneous Canine Malignancies. Clin Cancer Res 22:4328-40|
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