Endoscopic ultrasonography (EUS) was performed in 110 patients with gastric cancer to examine the depth of cancer invasion. The normal gastric wall has a five-layer structure on EUS. In 19 lesions, changes on EUS were limited to the first and/or second layers, suggesting that invasion was limited within the mucosa. In 91 lesions, changes were evident in the third or deeper layers. Alterations in the EUS appearance could be divided into two types: type A, with destruction of the layered structure and type B with thickening of the layers. The amount of interstitial tissue in cancer was classified as medullary or intermediate in 90% of type A, and as scirrhous in 82% of type B tumor. The EUS diagnosis of invasion was 95% accurate for stage M cancers, 75% for SM, 64% for PM, 100% for SS, 79% for SE, and 100% for SI lesions. The overall accuracy was 81%. Accompanying fibrosis and metastatic perigastric nodes were the main reasons for overestimating the extent of disease.

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Among 428 patients who had undergone absolute curative resection of gastric cancer, 57 died of cancer recurrence. One hundred and seventeen patients who had survived longer than 5 years were used as controls. In the recurrence group, the primary lesion was larger and the lymph node metastasis more common as compared with the surviving controls. Prognostic serosal invasion was positive in 74% of the recurrence group and negative in 85% of the surviving controls. The most frequent mode of recurrence was hematogenous metastasis in negative prognostic serosal invasion (75%) and peritoneal disseminated metastasis in positive prognostic serosal invasion (52%).

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The prognosis of early gastric cancer (EGC) is generally excellent, however, EGC is not an exception to recurrence. In order to know what type of EGC is liable to recur, long-term results were studied in 304 cases of resection. The cumulative 10-year survival rate was poorer in patients with positive lymph nodes than in those with negative nodes (52.8 +/- 15.8 per cent vs 94.1 +/- 2.4 per cent; p less than 0.05). It was also less favorable when the EGC was greater than 5 cm in diameter (61.5 +/- 13.2 per cent vs 92.9 +/- 2.4 per cent; p less than 0.05). Among 50 cases which died postoperatively, six deaths were due to recurrence. A predominant mode of recurrence was hematogenous metastasis (4/6). The characteristics of EGC which recurred later included large cancer (greater than or equal to 5 cm) (6/6), macroscopically combined-type cancer (5/6), cancer of depth invasion to the submucosa (4/6) and histologically differentiated cancer (6/6). Lymph node dissection was not carried out in two of these patients at their primary operation. Adjuvant therapy should be added in the EGC bearing risk factors depicted above. Primary cancer in other organs, either metachronous or synchronous, was found in 13 cases (4.3 per cent). Colonic cancer, in particular, was seen in three, and it was 4.8 times as frequent as the expected number of the general population, calculated using the person-year method.

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Summary An experimental trial in the induction of canine gastric cancers was conducted to study the relationship between the histological differentiation of adenocarcinoma and the duration of administration of the carcinogen, N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG). Twenty-three adult Beagle dogs were divided into three groups according to the duration of administration. Over 3 months administration, the total dose of ENNG per animal was 5.85 g, and only signet ring cell carcinomas and poorly differentiated adenocarcinomas were induced in the antral mucosa of the stomach in 5 of 10 recipients. During 6 and 9 months administration, the total doses per animal were 11.70g and 17.55g, well differentiated adenocarcinomas were observed in 12 of 13 animals and they coexisted with poorly differentiated adenocarcinomas and/or signet ring cell carcinomas. Atrophic hyperplastic gastritis and hyperplastic polyps were seen in the same stomach. The results of this study suggest that a greater amount of carcinogen, i.e., a higher total dose, is required for the development of well differentiated adenocarcinoma than for inducing poorly differentiated adenocarcinoma and signet ring cell carcinoma.