Hakan Cam, PhD
College of Medicine
Research Asst Professor
Molecular Biology and Cancer Genetics
Rhabdomyosarcoma, Anoxia, DNA Damage, DNA Breaks, Double-Stranded, Osteosarcoma, Neuroblastoma, Fanconi Anemia, Cell Transformation, Neoplastic
Cancer is a genetic disorder caused by mutations in genes critically involved in the control of cell proliferation. Long-lived organisms, such as humans, have evolved strategies to restrict the development of potentially malignant cells. The p53 family of tumor suppressor genes provides important defense against cancer. Activated in response to DNA damage and to oncogenic signaling the three proteins of this family - p53, p63 and p73 - cooperate to induce apoptosis and thus restrict tumor formation by eliminating potentially malignant cells. Importantly, alteration of this coordination often causes cancer. My lab is interested in: • How do p53 and its family members suppress tumorigenesis? • How do the p53 family inhibitors ?Np73 and ?Np63 enhance tumor formation? • How do the p53 family members regulate gene expression? • How do the p53 family members interact with other signaling networks? • What is the function of the p53 family members in normal development? Moreover, we focus on mTOR protein. Mammalian TOR (mTOR) is an evolutionarily conserved serine/threonine kinase that integrates signals from growth factors, nutrients, and stresses to regulate multiple processes, including mRNA translation, cell-cycle progression, autophagy, and cell survival. Body of evidence suggest that deregulation of mTOR pathway occurs in common diseases; including cancer and diabetes that emphasizes the importance of identifying and understanding mTOR signaling. Therefore, by using genetic approaches in both cell culture and animal models, my research goals are to understand and identify: how disruption of mTOR regulation can lead to pediatric diseases such as cancer.