Abstract
Colorectal cancer (CRC) develops through several histologically well-defined stages, reflecting the sequential acquisition of genetic alterations. Several frequently mutated genes have been identified which probably contribute to the development of both hereditary and sporadic cancer (reviewed in Bishop and Thomas, 1990; Fearon and Vogelstein, 1990; Fearon and Jones, 1992; Hamilton, 1992). Several generalizations emerge from this work. Mutations are observed in the earliest detectable stages of cancer development. Specific genes tend to be mutated in a given order, but it is the accumulation of a critical number of lesions which governs the appearance of neoplasia. Mutations actively promote neoplastic character by activating oncogenes and eliminate restraints on neoplastic character by inactivating tumour suppressor genes.
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