The Comparative Oncology Program of the University of California, Davis Cancer Center focuses on several specific aspects of cancer biology in animals. The first major theme, Tumor Biology, is the study of major Oncogenes, Tumor Suppressor genes. Cancer Stem Cells and Inflammation-Cancer. The second major theme. Genetically Defined Animal Models of Cancer, is the study of tumor development and progression employing transgenic and knockout animal models to elucidate basic mechanisms. The third major theme, Spontaneous Cancers in Large Animals, uses non-rodent animals to study tumor development and investigate novel diagnostics and therapeutics in a preclinical setting. This program brings a unique combination of skills and models to the preclinical setting. It provides the critical links between bench and bedside. The programmatic goals are: (1) to examine the signaling pathways of oncogenes and tumor suppressor genes and the role of inflammation and cancer stem cells in tumorigenesis using both in vitro systems and genetically defined animal models of cancer in vivo;(2) to characterize genetically induced tumorigenesis in animal models and development of novel animal models and experimental approaches;(3) to characterize spontaneous cancers in large animals and to perform preclinical evaluation of novel diagnostics and therapeutics;and (4) collaboration with other programs to facilitate translational research. The program has 29 members from ten different departments and three schools at UC Davis. It has 17 NCl funded projects for $2.6 million ADC (total peer-reviewed funding, $11.4 million ADC). The group has 524 publications for the last funding period;21% are inter-programmatic and 10% are intra-programmatic.
This program moves the discovery of new therapies for cancer by taking fundamental cancer discoveries and modeling them in mice. In addition, the program is unique in having 1300 patients (dogs and cats) that present with cancer to the veterinary school each year. By working together with colleagues treating human patients, the hope is to bring otherwise not available therapies to our veterinary patients, while speeding the discovery for new and effective therapies for our human patients.
|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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