Treatment of Gastric Neuroendocrine Tumors

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Abstract
GRIGIORI1 in 1985 was the first to divide gastric carcinoid tumors into 2 clinicopathologically distinct groups on the basis of the serum gastrin level. Although serotonin-producing enterochromaffin cells are rare in these tumors, the term gastric carcinoid is historically used in its nomenclature. Recently, gastric neuroendocrine tumors (gastric carcinoids) have been classified on the basis of pathogenesis and histomorphologic characteristics into 3 types differing in biological behavior and prognosis.2-8 Enterochromaffinlike (ECL) cells are the main endocrine cell types in type 1 and type 2 gastric neuroendocrine tumors and are highly susceptible to gastrin trophic stimulus. Under circumstances that cause hypergastrinemia, such as chronic atrophic gastritis (CAG) in pernicious anemia (type 1) or gastrin-producing neoplasms in Zollinger-Ellison syndrome (ZES)/multiple endocrine neoplasia (MEN) 1 (type 2), multiple ECL cell carcinoids occur in the oxyntic corpus and fundus mucosa of the stomach. Gastric neuroendocrine tumor types 1 and 2 are usually considered benign with a low risk of malignancy. Type 3 gastric neuroendocrine tumors are composed of different endocrine cells, including poorly differentiated endocrine and exocrine cells, which grow sporadically, irrespective of gastrin in an otherwise normal mucosa. Most of these tumors show a low- to high-grade malignant transformation, already metastasizing at the time of diagnosis.