Cancer is the end result of approximately eight contributing mutations in the tumor cell.
Such mutations affect pathways regulating cell proliferation, cell adhesion, cell cycle control, and other processes relating to tumor invasion and metastasis. However, these significant mutations are accompanied by vastly greater numbers of apparently superfluous mutations. Cancer now appears to represent the simple consequences of a natural selection process of accelerated somatic evolution involving cells with unstable genomes, with such selections giving rise to ordered pathways. Understanding how genomic instability arises at the molecular level, learning how genomic instability relates to the clinical course of the disease, and applying this knowledge to develop means of suppressing genomic instability in tumors are the principal objectives of our research group. The degree of genomic instability is being analyzed for correlation with various potential driving factors, including p53 mutation or expression of an anoxia-inducible endonuclease.