[ Summary ] |
In the 1970s, Muto and Morson clarified the theory that colorectal carcinogenesis was a multistep process, involving a number of morphologic steps, (the adenoma-carcinoma sequence). In 1988, Vogelstein et al. identified deletion and mutation of the APC gene, mutation of the K-rasgene, and abnormalities in the 17th and 18th chromosomes in colorectal multistep carcinogenesis as genetic models for the adenoma carcinoma sequence. On the other hand, Japanese endoscopists have found many non-polypoid (flat or depressed) colorectal cancers in the 1990s. Clinicopathologically, most non-polypoid colorectal cancers displayed symptoms of early invasion, in spite of their small size, endophytic growth, and lack of adenomatous components. The genetic backgrounds of non-polypoid colorectal cancers renain undoscovered, however, it is well known that APC and K-ras gene abnormalities are rare in non-polypoid colorectal cancers. These results suggest that the histopathological and genetical backgrounds of non-polypoid colorectal cancers differ from the adenoma-carcinoma sequence (de novo type carcinogenesis). In this paper, we described the morphogenesis and genetic backgrounds of various types of colorectal carcinogenesis (adenoma-carcinoma sequence, hereditary non polyposis colorectal cancer, colitis-dysplasia-colitic cancer sequence, de novo type carcinogenesis). |