A 67-year-old man visited a local hospital with abdominal pain. He underwent esophagogastroduodenoscopy (EGD), which revealed a 30 mm-sized elevated lesion with a concave surface and mucus production on the lesser curvature side of the middle of gastric body; however, the biopsy specimens obtained showed no malignant findings. The patient underwent another EGD the following month, and the biopsy specimens revealed pyloric adenoma (Group 3) with no malignant findings. The HE-stained specimen was positive for Helicobacter pylori infection, and he underwent the required eradication therapy.

Three months later, an EGD was restudied and biopsies were performed again; however, no malignant findings were observed. Then, the patient was referred to our hospital for a thorough examination of the lesion. An EGD revealed a 30-mm 0–IIa + IIc lesion with a depressed surface on the lesser curvature side of the middle of the gastric body (Fig. 1a, b). Magnifying narrow band imaging (NBI) revealed that the center of the lesion was white in color and vascularized (Fig. 1c). Endoscopic findings showed the good wall extensivity of the tumor, but the wall thickening remained by air suppression. Biopsy specimens revealed the presence of atypical cells and proliferating glandular ducts with irregular branching and fusion, raising suspicion of pyloric gland adenoma or pyloric gland adenocarcinoma. Endoscopic ultrasonography (EUS) showed isoechoic tumor with an elongated anechoic area, suggesting an ectopic pancreas. In addition, EUS findings showed the deep third layer and forth layer were remained, suggesting that the isoechoic tumor did not invade the deep submucosa and muscularis propria. Since it was hard to determine whether the lesion was benign or malignant, endoscopic submucosal dissection was performed. The resected specimen measured 68 × 50 mm. A 39 × 32-mm submucosal tumor (SMT)-like elevation was found, forming an ulcer measuring 26 × 17-mm (Fig. 2). Histopathologically, the lobular proliferation of pyloric grand-like acinar structures was observed but there were neither chief cells nor parietal cells. These atypical glands infiltrated the submucosal tissue (Fig. 3a–d). Venous invasion was observed (Fig. 3e). Immunohistochemically, tumor cells were positive for both MUC5AC and MUC6 (Fig. 3f and g), while pepsinogen-I and H+/K+-ATPase were both negative (Fig. 3h, i). The tumor’s Ki-67 labeling index was approximately 5% within the tumor (Fig. 3j). Contrast-enhanced computed tomography revealed no obvious lymph node or distant metastases. Based on the above, the patient was diagnosed with gastric adenocarcinoma of the pyloric gland type, pType 0-IIa + IIc, 39 × 32 mm, pT1b2(SM2) (2200 µm), UL0, Ly0, V1, pHM0, pVMX, cN0M0 cStage I. Due to submucosal layer infiltration and venous invasion, a laparoscopic distal gastrectomy with D1 + lymph node dissection was performed three months after the endoscopic submucosal dissection. The pathological findings of the resected specimen showed the absence of a residual tumor and no lymph node metastasis in 42 lymph nodes that were dissected. On postoperative day 3, the patient started oral intake, and he was discharged on postoperative day 7.

0–IIa + IIc lesion measuring 30 mm in size with a depressed surface at the lesser curvature side of the middle of the gastric body (a and b). Magnifying NBI revealed the vascular structure at the center of the lesion (c). Endoscopic ultrasonography revealed an isoechoic tumor with an elongated anechoic area suggestive of an ectopic pancreas, and also showed that the deep third layer and forth layer were remained (d)

Gross findings of the resected specimens by endoscopic submucosal dissection, measuring 68 × 50 mm in size, with a 39 × 32-mm SMT-like elevation, a 26 × 17-mm ulcer was observed on the side of the lesion (a–c)

Histopathological findings of the tumor. a–c Lobular proliferation of pyloric gland-like glands was observed. d Tumor glands infiltrated submucosal tissues. e Venous invasion was observed in Elastica van Gierson staining. f–i Immunohistochemical staining of MUC5AC (f) and MUC6 (g), Pepsinogen-I (h), and H + /K + -ATPase. (j) The Ki-67 labeling index of the tumor is approximately 5%