Popis: |
The c-myc gene plays a central role in a wide diversity of cellular processes, including cell cycle, cell growth (including protein synthesis), DNA dynamics, and apoptosis. As one of the most common oncogenes in human cancer, c-myc is commonly gene amplified in solid tumors and deregulated by chromosomal translocation in hematologic malignancies. A significant body of work has already defined pathologic effects of deregulated c-myc on cell proliferation, apoptosis, adhesion, and immortality in cancer. However, recent studies have begun to shed light on two, key, additional processes in cancer: cell transformation (anchorage independent growth), and genomic instability (including loss of cell cycle DNA damage-dependent checkpoint control). This review first covers structure-function relationships of c-myc; it then focuses on the emerging aspects of transformation and genomic instability in the pathophysiologic function of this very important oncogene. |