ABSTRACT
BACKGROUND: Some sporadic colon cancers and hereditary nonpolyposis colorectal cancer (HNPCC) have been known by a constitutional defect in mismatch gene repair (MMR) and dysfunction in of this MMR system, which lead to an aberrant phenotype that can cause microsatellite instability. However, the clinicopathologic features of still existing microsatellite stable (MSS) colon cancer remain to be investigated. METHOD: We compared the gene expression patterns of nine tumor tissues of HNPCC and nine tumor tissues of sporadic colon cancer with their adjacent pathologically normal, MSS tissues by modified differential display-polymerase chain reaction, selected four potential marker genes, and confirmed their reproducibility by reverse transcriptase-polymerase chain reaction. RESULTS: Reg I, MLCK, and MYH11 in tumors of MSS HNPCC showed significant differences in gene expression pattern compared with the adjacent pathologically normal tissues (P = 0.028, P = 0.002, and P = 0.001, respectively). Similar differences in expression patterns for the same set of genes were seen between the sporadic colon cancer group and their adjacent pathologically normal tissues (P = 0.012, P = 0.003, and P = 0.002, respectively). CONCLUSION: We suggest that the three cancer-associated differentially expressed genes in MSS sporadic colon cancer or MSS HNPCC might be potential tumor markers.
