The Kono-S anastomosis appears to be effective in preventing anastomotic surgical recurrence in Crohn's disease.

Syndecan-1 is a transmembrane heparansulfate proteoglycan which regulates cell-to-cell or cell-toextracellular matrix interactions and may influence malignant cell behavior. We investigated the alterations of syndecan-1 expressions in colorectal cancers and analyzed the relationship between histological and clinical characteristics. Syndecan-1 protein expression in colorectal cancer tissues was investigated with immunohistochemical staining of resected specimens. In situ hybridization was performed using syndecan-1 riboprobe to confirm the transcriptional signals. Syndecan-1 mRNA expression in cancer cell lines cultured with or without methylation inhibitor was also analyzed by quantitative PCR. Out of 105 specimens tested, less than 25% of tumor cells were stained with anti-syndecan-1 monoclonal antibody in 36 (34.3%). In situ hybridization showed a similar staining profile to that of immunohistochemistry. Syndecan-1 mRNA expression was increased by the methylation inhibitor 5-aza-2′ ′ ′ ′-deoxycytidine, suggesting that the hypermethylation is involved in the suppression of syndecan-1 expression. Clinically, the incidence of metastasis to lymphnode or liver in patients with syndecan-1-negative tumors was significantly high. Among T1 colorectal cancers displaying a primary invasive phase, lymphnode metastasis, undifferentiated characters and 'budding' of cancer cells were more common in syndecan-1-negative tumors. The survival rate in patients with syndecan-1-negative tumors was decreased significantly in a stage-independent manner. These results suggest that the reduction of syndecan-1 expression in colorectal cancer cells, which is supposed to be regulated at the transcription level, is closely related to invasive character. The evaluation of syndecan-1 expression in colorectal cancer may allow prediction of patients' survival after surgery.Key words: Syndecan-1 -Colorectal cancer -Metastatic potential -PrognosisGastrointestinal tract cancers disrupt the muscularis mucosa of the epithelia, with subsequent tumor outgrowth into the submucosal layer. When cancer cells are observed in the submucosal layer, invasion of lymphatic ducts or blood vessels is likely. Therefore, tumor cells in the submucosal layer have been considered to be an important pathological sign for predicting life-threatening metastasis. In order to disseminate into submucosal interstitial tissues, cancer cells must become detached from the tumor mass, 1) and this is closely associated with a reduction of cell-cell or cell-matrix adhesion.2) The disruption of cadherindependent cell adhesion has been extensively studied in relation to the progression or metastasis of colorectal cancers, but involvement of other molecules has not been reported.Recently, it has been suggested that syndecan, a family of transmembrane heparan sulfate proteoglycans, also plays an important role in the binding of tumor cells to extracellular matrix (ECM) molecules such as type I, III, V collagens, fibronectin, tenascin, and amphoterin on various cell lineages. Among s...

The Kono-S anastomosis appears to be safe and effective in reducing the risk of surgical recurrence in Crohn's disease.

To clarify field cancerization in the stomach by genetic alterations, we studied 83 cases of intestinal-type gastric cancer (GC) and paired intestinal metaplasia (IM) distant from GC and 39 cases of chronic gastritis with IM (CG-IM) for genetic instability (GIN). Microsatellite instability (MSI) and loss of heterozygosity (LOH) were evaluated at 5 microsatellite loci. The incidence of GIN was 21% (8/39) in CG-IM, 48% (40/83) in GC-IM, and 65% (54/83) in GC and showed a significant difference among these 3 categories. By tumor location, MSI showed the highest incidence in GC and GC-IM with the tumor located in the upper third of the stomach. GIN in GC and GC-IM significantly increased with the progression of tumor invasion from mucosal to advanced cancer. GIN, especially LOH, was more frequently detected in cases with vs without lymphatic or vascular invasion and lymph node involvement in GC and GC-IM. The GIN of GC and GC-IM was significantly similar in relation to clinicopathologic features. Biologic detection of GIN in IM may be a surrogate marker for GC risk and for clinical evaluation of malignant potential. The condition is consistent with the hypothesis of field cancerization in the stomach.

To clarify the biological impact and molecular pathogenesis of cellular phenotype in differentiated-type gastric cancers (DGCs), we investigated cell kinetics and genetic instabilities in early stage of DGCs. A total of 43 early gastric cancers (EGCs) were studied. EGCs were divided into 3 phenotypic categories: gastric (G type, n = 11), ordinary (O type, n = 20), and complete intestinal (CI type, n = 12) based on the combination of HGM, ConA, MUC2, and CD10. Proliferative index (PI), apoptotic index (AI), and p53 overexpression were investigated by immunohistochemical staining with anti-Ki-67, the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling method, and p53 antibody, respectively. Using a high-resolution fluorescent microsatellite analysis system, microsatellite instability (MSI) and loss of heterozygosity (LOH) were examined. Frameshift mutation analysis of transforming growth factor-beta type II receptor (TGF-betaRII) and bcl-2-associated X (BAX) in cancers with MSI was also performed. The mean AI/PI ratio values were 0.04 for G-type, 0.10 for O-type, and 0.13 for CI-type cancers--significantly lower in G type than in O and CI types (P = 0.02 and P = 0.001, respectively). No difference in the incidence of MSI and LOH was seen among the 3 cellular phenotypes. However, the major pattern of MSI, which showed drastic and widely dispersed changes and is related to an increased risk for cancer, was significantly higher in G and O types than in CI type (P <0.005). No frame shift mutations of TGF-betaRII or BAX were found in CI-type cancers. These results indicate that G-type cancers are likely to show more aggressive behaviors than CI-type cancers, and that O-type cancers show the intermediate characteristics of both types. However, the molecular pathogenesis of each phenotypic cancer is not associated with microsatellite alterations.