ABSTRACT
The application of rapidly evolving technology in the field of molecular biology has resulted in a decade of profound enlightenment concerning the identification of specific cellular abnormalities that contribute to malignant behavior. Evidence indicates that cancer is the result of a series of mutations within a defined subset of genes which are normally involved in the precise homeostatic control of cell replication and differentiation (1). In a remarkably short period of time, over 60 oncogenes and tumor-suppressor genes have been reported. We now have the technology to detect mutations in human tumor specimens resulting from a single base-pair substitution in a specific oncogene. These accomplishments are remarkable when we consider that the human genome contains over 1 × 105 genes and 1 × 109 base pairs. However, there remains a large gap between our knowledge of mutational events and our understanding of the subsequent steps leading to an invasive and metastatic cancer. An additional challenge for the next decade will be to define environmental and host factors which determine the frequency at which these cellular mutations accumulate and the rate at which they are expressed.
