ABSTRACT
Over the last two decades, molecular and genetic approaches have identified numerous molecules linked to carcinogenesis by virtue of their mutation in human tumors. These molecules have been classified as either oncogenes or tumor suppressor genes [1, 2]. Oncogenes are molecules that, when constitutively activated by mutation, promote neoplastic growth in a dominant manner. By contrast, tumor suppressor genes are genetically recessive-loss of function of these molecules enhances tumorigenesis. Since cancer results from net tissue expansion, much of cancer research has focused on how oncogenes and tumor suppressor genes regulate cell proliferation. Thus, considerable evidence indicates that oncogenes such as ras and cmyc normally function in signal transduction pathways that promote cell growth, whereas the products of several tumor suppressor genes (e.g. the retinoblastoma protein) play essential roles in negative growth control.
