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 #
3P30CA093373-10S2
Application #
8567249
Study Section
Subcommittee G - Education (NCI)
Project Start
2002-07-01
Project End
2016-06-30
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
10
Fiscal Year
2012
Total Cost
$75,000
Indirect Cost
$26,299
Name
University of California Davis
Department
Type
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
Zeng, Shu-Xiong; Zhu, Yanjun; Ma, Ai-Hong et al. (2017) The Phosphatidylinositol 3-Kinase Pathway as a Potential Therapeutic Target in Bladder Cancer. Clin Cancer Res 23:6580-6591
Zhong, Cheng; Han, Ju; Borowsky, Alexander et al. (2017) When machine vision meets histology: A comparative evaluation of model architecture for classification of histology sections. Med Image Anal 35:530-543
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(2017) New and emerging developments in extensive-stage small cell lung cancer therapeutics: Erratum. Curr Opin Oncol 29:88
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Jian, Chao; Tu, Mei-Juan; Ho, Pui Yan et al. (2017) Co-targeting of DNA, RNA, and protein molecules provides optimal outcomes for treating osteosarcoma and pulmonary metastasis in spontaneous and experimental metastasis mouse models. Oncotarget 8:30742-30755
Wan, Debin; Yang, Jun; Barnych, Bogdan et al. (2017) A new sensitive LC/MS/MS analysis of vitamin D metabolites using a click derivatization reagent, 2-nitrosopyridine. J Lipid Res 58:798-808

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