Ever since the discovery of oncogenes and tumor suppressor genes, it has been recognized that mutations in these genes could provide the initiation events for cancer. This discovery, therefore, linked mutagenesis to control of the cell cycle and to carcinogenesis. We now un- derstand that the development of a cell from normal to tumorigenic involves a sequence of mutational and chromosomal events. In 1990, Fearon and Vogelstein (1) reported that at least nine chromosomal alterations were found in up to 50/100 of colon adenocarcinomas in humans.
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