Sporadic pyloric gland adenoma associated with a large fundic gland polyp: genetic evidence for stepwise progression
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CASE REPORT
Sporadic pyloric gland adenoma associated with a large fundic gland polyp: genetic evidence for stepwise progression Satoru Nonaka1 · Taiki Hashimoto2 · Ichiro Oda1 · Shigeki Sekine2,3 Received: 25 March 2020 / Accepted: 3 May 2020 © The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2020
Abstract Pyloric gland adenoma (PGA) is an uncommon variant of gastric adenoma exhibiting pyloric gland/mucous neck cell differentiation. We present a sporadic PGA associated with a large fundic gland polyp (FGP) in a woman in her 40 s without Helicobacter pylori infection. The polyp, measuring 25 mm in size, was located in the middle gastric body and was removed by endoscopic submucosal dissection. Histological examination revealed three morphologically distinct components: FGP, FGP with large cysts, and PGA. A genetic analysis identified a truncating APC mutation in all the three components, supporting their histogenetic relationship. Additionally, a GNAS mutation was detected in two components, FGP with large cysts and PGA, whereas a KRAS mutation was exclusively found in the PGA component. Thus, despite the unusual presentation, the PGA component harbored prototypical genetic alterations. The differential genetic alterations observed in the three components imply that they represent stepwise progression from FGP to PGA. Keywords Pyloric gland adenoma · Fundic gland polyp · Genetic alterations
Introduction Pyloric gland adenoma (PGA) is an increasingly recognized variant of adenoma, most commonly located in the stomach and duodenum [1]. Gastric PGAs either occur sporadically or in patients with familial adenomatous polyposis (FAP) [2]. Sporadic gastric PGAs usually develop on a background of metaplastic mucosa due to Helicobacter pylori (H. pylori) infection or autoimmune gastritis [1, 2]. Despite its name, PGAs exhibit immunohistochemical profiles similar to mucous neck cells of fundic glands rather than pyloric glands, as indicated by the weak expression of pepsinogen-I in addition to diffuse MUC6 expression [3]. Consistently, PGAs are primarily located in the gastric body, which is normally covered by the fundic gland mucosa. Accordingly, it * Shigeki Sekine [email protected] 1
Endoscopy Division, National Cancer Center Hospital, 5‑1‑1, Tsukiji, Chuo‑ku, Tokyo 104‑0045, Japan
2
Division of Diagnostic Pathology, National Cancer Center Hospital, 5‑1‑1, Tsukiji, Chuo‑ku, Tokyo 104‑0045, Japan
3
Division of Molecular Pathology, National Cancer Center Research Institute, 5‑1‑1, Tsukiji, Chuo‑ku, Tokyo 104‑0045, Japan
is suggested that pseudopyloric metaplasia occurring in the fundic gland mucosa, which is induced by sustained inflammation, plays a critical role in the development of sporadic PGAs [3]. In contrast, FAP-associated PGAs are observed on the pristine fundic gland mucosa, often in association with fundic gland polyposis [4]. Fundic gland polyps (FGPs) in patients with FAP have clinicopathological features distinct from sporadic lesions [2]. They occu
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