Histogenesis and Genetic Changes of Gastric Neuroendocrine Tumors: Including MEN1 Gene Alteration Yasuharu Kaizaki 1 , Osamu Hosokawa 2 , Takeshi Fujii 3 , Takakiyo Nakaya 1 , Ken Saito 3 1Department of Pathology, Fukui Prefectural Hospital 2Departrnertt of Surgery, Fukui Prefectural Hospital 3Deportment of Pathology, Jichi Medical School Keyword: 胃カルチノイド , 胃神経内分泌癌 , 遺伝子異常 , MEN1遺伝子 pp.1355-1364
Published Date 2000/10/25
DOI https://doi.org/10.11477/mf.1403104890
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 Genetic pathways of gastric neuroendocrine tumors have not been fully clarified. We investigated the proliferative abilities and some of the oncogene expressions of gastric neuroendocrine tumors and reviewed reports on the genetic alterations. We classified the tumors into Type Ⅰ (associated with chronic atrophic gastritis type A, CAG/A), Type Ⅱ (associated with multiple endocrine neoplasms type Ⅰ), Type Ⅲ (sporadic), and Type Ⅳ (neuroendocrine carcinoma) according to Rindi's report. For the induction of Type Ⅰ, Ⅱ, the proliferation of enterochromaffin-like (ECL) cells is triggered by the trophic stimulus of hypergastrinemia, which occurs consistently in cases of CAG/A or Zollinger-Ellison syndrome. Reg gene mutation and overexpression of bcl-2 and basic FGF may lead the ECL cells to a state of hyperplasia. In addition, MEN1 gene mutation may represent the transforming event for the evolution from ECI. cell hyperplasia to neoplasia. For Type Ⅲ or Ⅳ, though further investigations are needed, the induction may be associated with p53 gene mutation or undetermined oncogenes in the X-chromosome.

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