Purpose: The aim of this study was to investigate the genetic alterations of early-stage nonfamilial colorectal carcinomas regarding microsatellite instability, with special reference to the shape of the tumors and the site of the lesions.
Methods: Formalin-fixed, paraffin-embedded specimens of 44 early-stage nonfamilial colorectal carcinomas were examined for microsatellite instability with use of polymerase chain reaction.
Results: The 44 carcinomas consisted of 16 flat carcinomas and 28 polypoid carcinomas. Nineteen carcinomas were located in the proximal colon (9 flat type and 10 polypoid type), whereas 25 were in the distal colon and rectum (7 flat type and 18 polypoid type). Ten (22.7 percent) of the 44 carcinomas had at least one positive locus, whereas five (11.4 percent) of them had two or more positive loci. In the proximal colon the percentage of flat carcinomas with at least one positive locus was significantly greater than that of the polypoid carcinomas (4/9 (44 percent) vs. 0/10; P = 0.04). Six patients had synchronous or metachronous colorectal carcinomas or both. They harbored microsatellite instability more frequently than patients with single colorectal carcinomas, and the differences were statistically significant (P < 0.02).
Conclusions: These data suggest that in nonfamilial carcinomas in the proximal colon, the genetic pathway in flat carcinomas may be different from that in polypoid carcinomas.