Group I pepsinogen (PG-I) staining was performed in the gastric carcinoma tissues of 75 patients by the peroxidase-antiperoxidase (PAP) method, 44 cases (59%) of which were positive for PG-I, suggesting that they were PG-I-producing gastric carcinomas. Type IV gastric carcinoma by the Borrmann classification and/or poorly-differentiated adenocarcinoma were positive for PG-I in high incidence. Serum and urinary levels of PG-I were determined by the Pepsinogen I Radioimmunoassay Kit in patients with gastric carcinoma who underwent total gastrectomy. The levels of PG-I declined remarkably or disappeared at 1 week after curative surgery. Changes of serum PG-I levels after total gastrectomy were observed in 9 patients with PG-I-producing gastric carcinomas, 7 of whom died of recurrence. The PG-I values became elevated with recurrence in 5 of them and the values increased with the passage of time. In contrast, no substantial changes in PG-I levels occurred in patients with no recurrence. These results suggest that PG-I is useful for the early detection of recurrent disease after total gastrectomy in patients with PG-I-producing gastric carcinomas.

Group I pepsinogen levels were determined in the homogenized supernatant of the lymph nodes with metastasis of the gastric carcinoma by radioimmunoassay. Mean levels of group I pepsinogen were 941 ng/g and some of the lymph nodes showed very high levels compared with those of non-metastatic lymph nodes, 269 ng/g. They were also significantly higher than those of the sera in the same sabjects, that is, the production of group I pepsinogen by gastric carcinoma was clarified.group I pepsinogen ; gastric carcinomaIt is generally accepted that the gastrointestinal carcinoma produces various proteins and some of them are available for clinical use as the tumor marker.This study was designed to elucidate whether group I pepsinogen found exclusively in the gastric mucosa (Samloff 1971) was produced also by gastric carcinoma cells. MATERIALS AND METHODSThirty-five metastatic lymph nodes of gastric carcinoma and 5 control lymph nodes without metastasis were obtained at surgery.They were rinsed in cold 0.1 M phosphate buffer, pH 7.2 and were homogenized in 10-20° in the same buffer with a ground homogenizer. Each homogenate was centrifuged at 26,000 X g at 4°C for 30 min and the supernatants were pooled and stored at -20°C.Group I pepsinogen levels of the supernatants were determined by Group I Pepsinogen Radioimmunoassay Kit (Cis Sorin, Green Cross Corp, Tokyo).The general scheme of the assay was that of a competitive binding, double antibody system. 125I-human group I pepsinogen and antiserum to human group I pepsinogen raised in rabbit were added to each sample with diluent buffer. They were mixed thoroughly using a mixer and were incubated overnight at room temperature.A precipitating reagent (antirabbit y-globulin goat serum) was added and mixed thoroughly.After the incubation for 15 min at room temperature, they were centrifuged for 20 min at 3,000 rpm. The supernatants were decanted by aspiration and the radioactivity of the precipitates was counted by a gamma scintillation counter.The sera of the 40 patients with gastric carcinoma were also prepared and the group I pepsinogen levels were determined by the same system.