2004 Volume 49 Issue 1+2 Pages 25-32
To clarify the relationship with development of colorectal cancer, we investigated chromosomal aberrations in 715 specimens of the colorectal neoplasm by cytogenetic analysis. A gain of chromosome 17 was observed in the transitional epithelium around non-polypoid carcinomas, although the normal epithelium exhibited diploidy. Most tubular adenomas were diploid, however, loss of chromosome 11 and gain of chromosome 17 were increased in adenomas in association with an increased villous component. DNA aneuploidy, aneusomy and p53 deletion were predominantly observed in carcinomas, even in early cancers. Alterations of chromosomes 11 and 18 reflected different tumor morphologies in the early carcinomas. Gains of chromosomes 11, 17 and 18, and deletion of chromosomes 11 and 17p and p53 became more frequent following an increase in the depth of invasion. Aneusomy of chromosome 11 was a risk factor for patient survival after operation. Gains of chromosome 20 and 20q13.2 were associated with liver metastasis. Aneusomy and translocations of chromosome 17 and the p53 locus were predominantly observed in patients with multiple cancers and hereditary non-polyposis colorectal cancer. Our results indicate that in the process of development of colorectal carcinomas, specific chromosomal aberrations might be related to each step of development, or an alternative pathway of de novo carcinogenesis.