Analysis of Cell Proliferation in Endoscopically Biopsied Specimens of Stomal Mucosa of the Gastric Remnant

Abstract

Carcinoma of the gastric remnant is thought to occur more commonly in the stomal than in the other areas, particularly following Billroth II surgery (BII). An attempt was made to determine the status of cell kinetics in the gastric remnant using endoscopically biopsied specimens, with assay of ornithine decarboxylase (ODC) activity and flow cytometric analysis of the cell cycle parameters. Fifty‐two partially gastrectomized patients were studied. Significantly higher ODC activity was recognized in the stomal mucosa than in the greater curvature; this difference was especially pronounced for the group of BII patients. The S‐phase cell percentage was also significantly higher in the stomal area than in the greater curvature; this was particularly so in the patients who had undergone BII 5 or more years prior to this study. Our results suggest that activation of cell proliferation is present in the stomal area of the gastric remnant following BII surgery. This activation increased with time following surgery. Activation of cell proliferation occurred in association with histological changes in the stomal glands, and may play a role in carcinogenesis within the gastric remnant.

Frequent p16 CpG island hypermethylation in primary remnant gastric cancer suggesting an independent carcinogenic pathway

“…Based on the present results we suggest that there are different molecular pathways in carcinogenesis of the remnant stomach after surgery for benign disease compared with that after cancer surgery, as has been demonstrated in many clinical investigations (7,26). Furthermore, as Klump has suggested (39), the promoter methylation status may be a candidate marker for diagnosis and for clinically unapparent neoplastic alterations in patients with remnant stomach.…”

“…The influence of reflux of the duodenal juice on cancer development at anastomosis of the remnant stomach in animal models is well known (4). We have also observed the acceleration of glandular hypertrophy and cellular proliferation at anastomosis in clinical samples more predominantly in Billroth II type reconstruction, where reflux is more commonly found than in Billroth I type reconstruction (24)(25)(26). Kaminishi et al have reported that surgical denervation impairs the defense mechanism in the mucosa at the stump of the remnant stomach, leading to tumor development in experimental models (5).…”