Gene Regulation and Microsatell ite Instabil ity of the COX-2, hMLH1 and hMSH2 in Gastric Carcinoma

Objective 　To investigate the COX-2, hML H1 and hMSH2 of genes promoter methylation and MSI frequency in 43 cases of human gastric carcinoma and normal tissues, and to evaluate the relationship between them and occurrence of gastric carcinoma. Methods 　Methylation specific PCR (MSP) and polymerase chain reaction ( PCR) methods were employed in this study in order to investigate the promoter methylation of these genes and 5 loci MSI f requency in human gast ric carcinoma and normal tissues. Results 　Of 43 gast ric carcinoma cases, the total f requency of MSI was 48. 84 % (21/ 43) . The MSI frequency no significant discrepancy was found among the 5 loci. Cases with methylation of COX-2 and hMLH1 gene promoter Cp Gislands in gastric carcinoma were 8 and 13, and they were not detected in normal tissues. Methylation of hMSH2 gene promoter Cp Gislands was not detected in gastric carcinoma or normal tissues. The methylation rate of hML H1 gene promoter Cp G islands in MSI-H was higher than that in MSS ( P < 0. 01) . There was no significant difference between MSI-H and MSI-L, and the same result was found between MSI-L and MSS. 8 cases with methylation of COX-2 gene promoter Cp Gislands only occurred in MSI-H gast ric cancer, and 7 cases both with methylation of COX-2 and hML H1 gene promoter Cp G islands was observed in MSI2H. Conclusion 　Methylation of hML H1 and COX-2 gene promoter Cp Gislands may both occur in the development of MSI gastric carcinoma. The methylation rate of hMLH1 gene promoter Cp Gislands in MSI gastric carcinoma was higher than that in MSS gastric carcinoma. It suggested that detecting the methylation of hMLH1 gene promoter Cp Gislands might be a useful method for determining the gast ric carcinoma type.