Ken Kumagai, Takahiro Shimizu, Mitsuhiro Nikaido, Tomonori Hirano, Nobuyuki Kakiuchi, Yasuhide Takeuchi, Sachiko Minamiguchi, Takaki Sakurai, Mari Teramura, Takahiro Utsumi, Yukiko Hiramatsu, Yuki Nakanishi, Atsushi Takai, Shin'ichi Miyamoto, Seishi Ogawa, Hiroshi Seno
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{"title":"On the origin of gastric tumours: analysis of a case with intramucosal gastric carcinoma and oxyntic gland adenoma","authors":"Ken Kumagai, Takahiro Shimizu, Mitsuhiro Nikaido, Tomonori Hirano, Nobuyuki Kakiuchi, Yasuhide Takeuchi, Sachiko Minamiguchi, Takaki Sakurai, Mari Teramura, Takahiro Utsumi, Yukiko Hiramatsu, Yuki Nakanishi, Atsushi Takai, Shin'ichi Miyamoto, Seishi Ogawa, Hiroshi Seno","doi":"10.1002/path.6050","DOIUrl":null,"url":null,"abstract":"<p>Most gastric cancers develop in inflamed gastric mucosa due to <i>Helicobacter pylori</i> infection, typically with metaplastic changes. However, the origins of gastric cancer remain unknown. Here, we present a case of intramucosal gastric carcinoma (IGC) and oxyntic gland adenoma (OGA) derived from spasmolytic polypeptide-expressing metaplasia (SPEM). Early gastric cancer adjacent to a polyp was found in the upper corpus of a 71-year-old woman without <i>H. pylori</i> infection and was endoscopically resected. Histological examination showed IGC and OGA, both of which had predominant MUC6 expression. Interestingly, gastric glands with enriched MUC6-positive mucous cells, referred to as SPEM, expanded between them. Whole-exome sequencing analysis revealed a truncating <i>KRAS</i>(G12D) mutation in IGC, OGA, and SPEM. In addition, <i>TP53</i> and <i>CDKN2A</i> mutations and a loss of chromosome 17p were found in the IGC, whereas a <i>GNAS</i> mutation was observed in the OGA. These results indicated that IGC and OGA originated from the <i>KRAS</i>-mutated SPEM. © 2023 The Pathological Society of Great Britain and Ireland.</p>","PeriodicalId":232,"journal":{"name":"The Journal of Pathology","volume":"259 4","pages":"362-368"},"PeriodicalIF":5.6000,"publicationDate":"2023-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Pathology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/path.6050","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
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Abstract
Most gastric cancers develop in inflamed gastric mucosa due to Helicobacter pylori infection, typically with metaplastic changes. However, the origins of gastric cancer remain unknown. Here, we present a case of intramucosal gastric carcinoma (IGC) and oxyntic gland adenoma (OGA) derived from spasmolytic polypeptide-expressing metaplasia (SPEM). Early gastric cancer adjacent to a polyp was found in the upper corpus of a 71-year-old woman without H. pylori infection and was endoscopically resected. Histological examination showed IGC and OGA, both of which had predominant MUC6 expression. Interestingly, gastric glands with enriched MUC6-positive mucous cells, referred to as SPEM, expanded between them. Whole-exome sequencing analysis revealed a truncating KRAS (G12D) mutation in IGC, OGA, and SPEM. In addition, TP53 and CDKN2A mutations and a loss of chromosome 17p were found in the IGC, whereas a GNAS mutation was observed in the OGA. These results indicated that IGC and OGA originated from the KRAS -mutated SPEM. © 2023 The Pathological Society of Great Britain and Ireland.