Molecular genetic changes in benign colorectal tumors synchronous with microsatellite unstable carcinomas do not support a field defect.

backgroundA colorectal cancer may develop through a particular molecular genetic pathway, raising the question of whether the particular molecular changes are random, or are unique to the particular segment of colon. We wanted to determine whether molecular changes found within a colorectal cancer might also be detected in separate adenomas and polyps removed from the same area of colon at surgery. Microsatellite instability was chosen as a marker for a pathway of colon carcinogenesis.

methodsWe studied a total of 46 primary colorectal cancers with microsatellite instability and 77 synchronous adenomas and polyps. All tumors were evaluated for microsatellite instability,

resultsForty-nine benign tumors did not follow a pathway similar to that of their 31 synchronous primary cancers. For two distinct subsets of the microsatellite unstable colorectal cancers, those with acquired methylation and

conclusionsThese differences suggest a stochastic process within the colon regarding the particular molecular carcinogenic pathways followed by the synchronous tumors, rather than a 'field defect' within the colon segments. Variability in molecular findings was present for colorectal cancers arising from acquired methylation, as well as those cancers suggestive of a germ line origin.