[Findings of genetic changes in small intestinal carcinomas]

There is now good evidence that a series of genetic lesions in both dominant oncogenes and tumor suppressor genes are involved in the pathogenesis of human digestive tract carcinomas. Small intestinal carcinomas are very rare, accounting for only about 0.19% of all primary gastrointestinal malignant tumors in Japan, so there are few reports investigating genetic changes of small intestinal carcinoma. We analyzed 3 microsatellite loci and the status of K-ras and p53 genes isolated from tumors and surrounding normal tissue samples obtained during surgery. The polymerase chain reaction (PCR) technique used frequent genetic instability to assess differences between tumor and matched DNAs. Replication errors (RERs) were observed in 3 of the 29 cases (10%) of gastric carcinoma and in 11 of the 72 cases (15%) of colorectal carcinoma. None of the 13 (0%) esophageal carcinoma cases showed any RER, but 5 of 11 cases of small intestinal carcinoma (45%) had RERs, reflecting a significantly high incidence. None of the 11 small intestinal carcinoma cases exhibited K-ras gene mutations. Of 7 case amplified successfully by polymerase chain reaction (PCR) in exon 5-8 loci in p53 gene, 2 exhibited abnormally migrated bands in polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis. It is thus clear that the genetic carcinogenesis in the small intestine is different from other parts of the digestive tract. These results suggest that genetic instability plays an important role in the pathogenesis of small intestinal carcinomas.