The Molecular Oncology Program of the University of California, Davis Cancer Center is focused on understanding fundamental processes associated with carcinogenesis and the molecular and cell biology of cancer cells. Within this framework the program integrates two distinct but related and mutually reinforcing areas, oncogenic signals and chromosome biology. Of particular interest is how cellular signals regulate chromatin remodeling with respect to the assembly of nuclear hormone receptors and DNA repair complexes. Genome instability is a common denominator for most, if not all, cancers, and misregulated signaling pathways are often the root cause for malignant transformation. Two central themes, 1) Cytoplasmic Signaling and Chromosome Dynamics and 2) Nuclear Signaling and Chromosome Stability, integrate a distinguished group of investigators. The programmatic goals are: 1) Discovery of critical molecules involved in the signaling to and function of transcriptional and DNA repair/recombination complexes In cancer cells;2) Identification of critical molecules in signaling and function of transcription and DNA repair as potential predictive markers and therapeutic targets in cancer;3) Collaboration with other programs to facilitate translational research originating in the basic scientific discoveries of the Molecular Oncology Program. The program has 35 members from 10 different academic units of UC Davis and LLNL. It has 16 NCl-funded projects for $2.4 million ADC (total peer-reviewed funding, $10.7 million ADC). The group has 449 publications for the last funding period;22% are inter-programmatic and 10% are intra-programmatic

Public Health Relevance

): To Improve survival from cancer, more fundamental information must be gained. This program contributes to this task by discovering how cells alter the way In which they signal as they move from normal to cancer. The program also focuses on understanding how DNA Is repaired. DNA repair may initially stop cancers developing;however, after cancer is present, alterations in DNA repair may influence the tumor's response to therapy.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA093373-12
Application #
8743639
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
12
Fiscal Year
2014
Total Cost
$19,487
Indirect Cost
$6,792
Name
University of California Davis
Department
Type
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
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
Taché, Véronique; 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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