Abstract
Microsatellite instability characterizes a sub‐set of sporadic colorectal cancers (CRCs) as well as CRCs from patients with hereditary non‐polyposis colorectal cancer (HNPCC). In order to clarify when the cells acquire a replication‐error phenotype (RER) during colorectal‐tumor progression, we examined the incidence of RER in 80 primary tumors and 36 liver metastases at 8 microsatellite loci; I mono‐, 5 di‐, I tetra‐ and I penta‐nucleotide. RER were detected in 20.1% (17/80) of primary tumors, including 5 tumors showing RER at 2 or more loci (RER2), while the incidence of RER in liver metastases (22.2%, 8/36) was almost the same as that in primary tumors, and there was only one RER2 case in metastases. There were 3 cases in which both primary tumors and liver metastases had the same type of RER at the same locus, and there were 2 cases that showed RER in primary tumors but not in liver metastases. In contrast, there was no case in which RER was detected in a metastasis but not in the corresponding primary tumor. The RER phenotype did not show correlation with any clinicopatho‐logical parameters of cancer‐cell aggressiveness, such as clinical staging, histological grade and survival. These results indicate that a sub‐set of CRCs acquire the RER phenotype in the relatively early stages of colorectal carcinogenesis, and that the RER phenotype is not associated with aggressiveness of CRCs. © 1995 Wiley‐Liss, Inc.