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Background. Matrix metalloproteinase-7 (MMP-7) is a member of the family of matrix-degrading metalloproteinases (MMPs) that are considered to contribute to cancer invasion and metastasis. One of the gene products that the authors have isolated by a cDNA subtraction of human gastric cancer minus normal gastric mucosa is MMP-7. The purpose of this study was to examine the expression of MMP-7 mRNA in different stages of human colorectal carcinomas. Methods. A subtracted complementary DNA library was generated from a paired sample of human gastric carcinoma minus normal gastric mucosa. Screening of the library clones determined that MMP-7 mRNA was overexpressed. The complementary DNA insert was then used as a probe to evaluate the expression in a larger number of surgical samples of human colorectal carcinomas by Northern hybridization. Results. The mRNA signal was greater in the colorectal carcinoma than in paired adjacent normal colonic or rectal mucosa in 39 of 47 cases. The expression of MMP-7 mRNA in tumor tissues increased with increasing Dukes' stage (P < 0.05). The MMP-7 mRNA expression was greatest in the metastatic liver lesions. Conclusions. The findings imply that MMP-7 mRNA is overexpressed in human colorectal carcinomas and that MMP-7 may prove useful as a marker of biologic aggressiveness. Cancer 1995;75:1516-9.

Background. Recent studies have shown that microsatellites are unstable in various types of cancers, and such genetic instability at the microsatellite loci (microsatellite instability) has been considered to play an important role in the development of cancer. However, the clinicopathologic significance of microsatellite instability in gastric cancer has not been clarified. Methods. To elucidate the role of genetic instability in the development of gastric cancer, the presence of microsatellite instability was examined in 25 cases of gastric cancer using fresh-frozen tumor-normal paired samples using a polymerase chain reaction (PCR)-based method. Microsatellite instability was defined as tumors that showed altered banding patterns at two or more microsatellite loci. Results. The incidence of microsatellite instability in gastric cancer cases was 4 of 25 patients (16%) and 4 of 26 cancers (15%). A significantly high incidence of microsatellite instability was observed in both the elderly (P < 0.01) and in lymph node metastasis-negative patients (P

Background. N-acetylation polymorphism has been documented as a representative pharmacogenetic trait, and also has been implicated ecogenetically in an individual's susceptibility to cancer. However, there still remains controversy concerning the association between colorectal cancer and N-acetylation polymorphism. Methods. A newly established molecular genotyping method using polymerase chain reaction-based restriction fragment length polymorphism to analyze the distribution of polymorphism in a large group of japanese patients with colorectal cancer was used. Results. Based on an analysis of 234 Japanese patients with colorectal cancer and 329 healthy control subjects, no significant difference was observed in either the distribution of acetylator phenotypes or of allele frequencies between the two groups. In addition, no significant difference in their distribution was found based on the age at which cancer was first detected, the location of tumors, or the histopathologic features. Conclusions. N-acetylation polymorphism does not appear to be implicated crucially as a genetic trait affecting an individual's susceptibility to colorectal cancer.

We developed a reliable procedure for obtaining sufficient blood flow at the anastomotic site of the gastric tube for esophageal reconstruction. By utilizing the junction between the left gastroepiploic and short gastric vessels via the splenic hilar vascular arcade, the distal portion of the gastric tube could be sufficiently nourished. The application of this technique resulted in a complete prevention of postoperative anastomotic leakage after antesternal esophageal reconstruction.

The chronologic changes in the serum levels of interleukin-6 (IL-6), a mediator for acute-phase inflammation, were compared between laparoscopic cholecystectomy (LC) and open cholecystectomy (OC), since these two types of operations were considered to be a unique model for examining the role of local tissue injury in postoperative inflammatory reactions. The increase in the serum IL-6 level during LC was found to be significantly smaller than that during OC and resulted in a smaller extent of postoperative elevations for C-reactive protein. These results suggest that laparoscopic surgery associated with minimal tissue injury can help limit an increase in the serum IL-6 level during surgery, thus contributing to a reduction in surgical stress.