Abstract
Almost 20% of colon cancers are characterized by genomic instability at simple repeated sequences. This instability is the result of a deficient DNA mismatch repair system. Sporadic, as well as hereditary carcinomas of the proximal colon display this effect. In this study, we examined colorectal adenocarcinoma cell lines, with or without wild-type adenomatous polyposis coli (APC) protein, for the presence of microsatellite instability. The three cell lines that maintained full-length APC protein also displayed the highest level of instability, suggesting a negative correlation between APC mutations and microsatellite instability. This data, in addition to other studies that show a negative correlation between microsatellite instability and mutations in p53 and K-ras, support the idea of a second pathway for colorectal cancer development.
Footnotes
-
↵1 This work was supported by The American Gastroenterological Association Foundation, The Council for Tobacco Research, Inc. (SA023), The Elsa U. Pardee Foundation, and NIH Grant CA-63507.
-
↵2 To whom requests for reprints should be addressed.
- Received July 26, 1995.
- Accepted September 12, 1995.
- ©1995 American Association for Cancer Research.
Volume 55, Issue 21
