Effects of telomerase and intracellular signal transduction pathways on carcinogenesis and development of colorectal carcinoma

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Telomeres of somatic cells are shortening with each cell division. While telomerase which involve the maintenance of telomere length is activated in malignant cells, and as a result, such cells aquire immortality. Mutations in mismatch repair genes result in a mutator phenotype that can be identified by observing microsatellite loci in nonfamilial colorectal cancer as well as hereditary non polyposis colorectal cancer. In this study, we investigated the telomerase activity and the microsatellite instability in nonfamilial colorectal cancers and adenomas. Telomerase activity was detected in 75% of colorectal cancers and in 33% of adenomas. Microsatellite instability was detected in 24% of sporadic cancers, in 54% of multiple cancers, and in 22% of colorectal adenomas. Telomerase activity and microsatellite instability ware independent events in colorectal carcinogenesis. The patients with telomerase activity and microsatellite instability showed poor prognosis. These results indicate that colorectal cancers with both telomerase activity and microsatellite instability may have more malignant potential, and adenomas with both telomerase activity and microsatellite instability may be more intensive precursor of colorectal cancers.