In recent years, there has been considerable progress in understanding the molecular events that give rise to clonal tumor development. This is best described by the steps in the development of colorectal tumors in which the activation of cellular protooncogenes and inactivation of several tumor suppressor genes has been elucidated (1 ). The well- defined steps in the development of these tumors from normal epithelium through adenomas or benign tumors to carcinomas has now been paralleled by identification of several genetic loci which are mutated as the tumor develops.
