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.
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.
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