A c-Myc and N-Myc double knockout P6 cerebellum, stained in green for the tumor suppressor p27KIP1, exhibits dramatically elevated KIP1. This data from the Knoepfler Laboratory suggest that excess Myc may cause the pediatric brain tumor medulloblastoma in part through suppressing KIP1 leading to cancer stem cell formation.
The NIH funded T32 fellowship program in Oncogenic Signals and Chromosome Biology (OSCB) has developed from a general interest in cellular responses and signal pathways integrating both responses to the cellular environment mediated by cell surface receptors and to signals initiated inside of the cell nucleus such as damage to DNA. While diverse in nature, these signals are often inseparable and interconnected by kinases and cascades of phosphorylation. The majority of the research projects among Mentors in the OSCB Fellowship Program involve detailed mechanistic studies in vitro which complement in vivo studies using animal models. Mentors are drawn both from the UC Davis cancer research community and from scientists at the Lawrence Livermore National Laboratory; a formal collaborative agreement brings the two institutions together for cancer-related research.