A genetic model for colorectal tumorigenesis

Abstract

Tumorigenesis has long been thought to be a multistep process (Foulds, 1958); however, only recently has it become possible to identify the molecular events that underlie the initiation and progression of human tumors (Weinberg, 1989; Bishop, 1987). Colorectal tumors provide an excellent system in which to search for and study the genetic alterations involved in the development of a common human neoplasm. Abundant clinical and histopathological data suggest that most, if not all, malignant colorectal tumors (carcinomas) arise from preexisting benign tumors (adenomas) (Sugarbaker et al., 1985). Tumors of various stages of development, from very small adenomas to large metastatic carcinomas, can be obtained for study, unlike the situation in most other common human tumor types. Furthermore, both hereditary and environmental factors contribute to the development of colorectal neoplasia, allowing for the study of both inherited and somatic genetic alterations.