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تسجيل

Gastrinoma : Pathophysiology and Molecular Pathogenesis

المؤلف:  Wass, J. A. H., Arlt, W., & Semple, R. K. (Eds.).

المصدر:  Oxford Textbook of Endocrinology and Diabetes

الجزء والصفحة:  3rd edition , p999-1000

2026-08-25

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Gastrinomas secrete mainly the carboxy- amidated- gastrin- 17, which is associated with gastric acid hypersecretion and relevant clinical features. This autonomous hypergastrinaemia induces ECL cell hyperplasia, which may lead to the development of gastric neuroendocrine tumours (Figure 1). Apart from amidated gastrin, these tumours may also secrete precursor forms, progastrin, and glycine- extended gastrin. Gastrinomas overexpress various growth factor receptors (epidermal growth factor receptor, insulin growth factor 1 receptor and hepatocyte growth factor receptor) but among these, only epidermal growth factor receptor (EGFR) is known to correlate with angioinvasion. The activation of CCK- 2 receptor by carboxy- amidated- gastrin- 17 initiates multiple signal transduction pathways, including activating EGFR.

Fig1. Pathophysiology of type II gastric carcinoids within the context of gastrinomas associated with MEN- 1 syndrome. Gastrinomas usually located inside the gastrinoma triangle (duodenum or pancreas) secrete excess amount of gastrin (1). Gastrin stimulates parietal cells to secrete gastric acid (2). Gastrin also stimulates mucosal growth in the stomach causing ECL cell hyperplasia (3), which can then lead to the formation of a neuroendocrine tumour (gastric carcinoid type II). Reproduced with permission from Grozinsky- Glasberg S, Alexandraki KI, Angelousi A, Chatzellis E, Sougioultzis S, Kaltsas G. Gastric Carcinoids. Endocrinol Metab Clin North Am. 2018 Sep;47(3):645– 60. Copyright © 2018 Elsevier Inc.